i

,

Digitally Signed by: Content manager’s Name

DN : CN = Webmaster’s name

O = University of Nigeria, Nsukka

OU = Innovation Centre

Agboeze Irene E.

FACULTY OF VETERINARY MEDICINE

VETERINARY PATHOLOGY AND MICROBIOLOGY

CUTANEOUS AND SYSTEMIC PATHOLOGIC

RESPONSES OF THE WEST AFRICAN DWARF GOAT TO

SARCOPTES SCABIEI INFESTATION

ONOJA, IBE REMIGIUS

PG/M.Sc/09/52104

i

CUTANEOUS AND SYSTEMIC PATHOLOGIC RESPONSES OF THE

WEST AFRICAN DWARF GOAT TO SARCOPTES SCABIEI INFESTATION

BY

ONOJA, IBE REMIGIUS

PG/M.Sc/09/52104

DEPARTMENT OF VETERINARY PATHOLOGY AND MICROBIOLOGY

FACULTY OF VETERINARY MEDICINE

UNIVERSITY OF NIGERIA, NSUKKA

AUGUST, 2013

ii

CUTANEOUS AND SYSTEMIC PATHOLOGIC RESPONSES OF THE WEST

AFRICAN DWARF GOAT TO SARCOPTES SCABIEI INFESTATION

BY

ONOJA, IBE REMIGIUS

DVM (Nig)

PG/M.Sc/09/52104

A DISSERTATION

SUBMITTED TO THE DEPARTMENT OF VETERINARY PATHOLOGY AND

MICROBIOLOGY, FACULTY OF VETERINARY MEDICINE, UNIVERSITY OF

NIGERIA, NSUKKA FOR THE AWARD OF THE DEGREE OF MASTER OF

SCIENCE

AUGUST, 2013.

iii

DECLARATION

The work presented in this dissertation is original and was done by me under the

supervision of Prof. S. V. O. Shoyinka. References made to the works of other investigators

were duly acknowledged. No part of this dissertation has been submitted for any other

diploma or degree of this or any other University.

ONOJA, IBE REMIGIUS

__________________________

DATE

UNIVERSITY OF NIGERIA, NSUKKA

iv

CERTIFICATION

Dr. Onoja, Ibe Remigius, a postgraduate student in the Department of Veterinary

Pathology and Microbiology and with Reg. No. PG/M.Sc/09/52104 has satisfactorily

completed the requirements for the course and research work for the degree of Master of

Science in Veterinary Pathology. The work embodied in this dissertation is original and has

not been submitted in part or full for any other diploma or degree of this or any other

University.

________________________

Prof. S. V. O. Shoyinka (Supervisor)

____________________ ________________________

External Examiner Prof. K. F. Chah (Head of Department)

____________________________

Prof. S. V. O. Shoyinka (Dean, Faculty of Veterinary Medicine)

v

DEDICATION

This effort is dedicated to Almighty God who through various individuals made this

programme successful. The world is a time clock and no one ever achieves unless it is God’s

time for one to do so.

vi

ACKNOWLEDGMENT

A lot of people have intentionally or unintentionally contributed to the success of this

programme and research work. Worthy of note in this regard is my wonderful mentor, teacher

and supervisor, Professor S. V. O. Shoyinka. He not only supervised this work but offered me

an informal scholarship to run this programme. He is second to God in my life and though I

am not fit to pay him back, his actions demands of me to reciprocate same to others.

Although an appreciation of my supervisor sums up my earnest wish for

acknowledgement, it is morally right that I recognize my wonderful teachers and colleagues

who had affected me positively. Thus, I will like to say thank you to Profs, C. N. Chineme, J.

I. Ihedioha, K. F. Chah, I. C. Nwaogu, V. O. Anosa, Dr. R. Antia (of the University of

Ibadan who kindly obliged my request to learn some aspects of Exfoliative cytology during

his College of Veterinary Surgeons, Nigeria lectures), A.O. Anaga and Drs C. Ezema, C.

Igbokwe, T. Nnaji, S. O. Udegbunam, W. S. Ezema, C. Okorie-Kanu, G. C. Okpe, D. C. Eze,

Idika K. Idika, C. Iheagwam, R. I. Obidike, Dr Obasi, C. N. Okoye and others too numerous

to mention.

I am also grateful to my brothers and sisters for their wonderful support and

encouragement.

vii

ABSTRACT The pathophysiology of Sarcoptes scabiei infestation in the West African Dwarf goat was

evaluated in a natural transmission study. Twenty- five adult male West African Dwarf

(WAD) goats consisting of 15 naturally infested goats assigned into three equal groups based

on severity of clinical disease as: A (mild infestation), B (moderate infestation), C (severe

infestation), and10 healthy WAD goats with no previous history of mange infestation

assigned into two equal groups as D (for contact transmission experiment) and uninfested

control (E) were used for this study. Parameters assessed at the beginning of the study (week

0) and every two weeks thereafter included packed cell volume (PCV), haemoglobin

concentration (Hb), erythrocyte count (EC), mean corpuscular volume (MCV), mean

corpuscular haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC),

total leucocyte count (TLC), differential leucocyte count (DLC), total protein, serum

albumin, creatinine, adrenal and gonadal steroid hormones concentration (cortisol and

testosterone), serum copper, zinc and vitamin A concentrations. At week 6 of the study, goats

in the five groups were sacrificed and the testicular and epididymal sperm reserves were

determined. Tissue sections of the infested skin of goats from groups A, B, C, D, and the

normal control E were processed for histopathological studies. Data generated were analyzed

using one-way analysis of variance (ANOVA), and variant means were separated using the

Duncan’s multiple range test. Significance was accepted at p < 0.05.

There was wide variation in the susceptibility and severity of infestation in the group

D goats (in-contact) as only three out of the five goats showed clinical signs of disease by the

6th

week while mite was only demonstrated in two out of five by the 6th

week. Lesions were

anterio-posterior in distribution. There were significant (p < 0.05) reductions in PCV, Hb and

EC mean values of the goats naturally infested with Sarcoptes scabiei in groups A, B and C

relative to uninfested control group E at weeks 0, 2 and 4, but at week 6 all the infested

viii

groups including in-contact group D had a significantly (p < 0.05) lower PCV, Hb and EC

compared to the control group E. There were no significant (p > 0.05) differences in some

erythrocytic indices (MCV, MCH, MCHC) among the five groups of WAD goats. However,

there was a significant (p < 0.05) increase in mean TLC in groups B and C compared to

groups A, D and the control, E. The increase in TLC was accompanied by a significant (p <

0.05) increase in both the absolute neutrophil and lymphocyte counts in groups B and C

compared to groups A and E. Significant (p < 0.05) difference in the mean monocyte count

was only observed among the groups at week 6 in the group C compared to A, B, D and E.

There was a significant (p < 0.05) increase in mean eosinophil count in groups A and B

compared to groups C, D and E throughout the period of study. Serum biochemical assay

showed significant (p < 0.05) reduction in mean total protein in severely infested group C

compared to groups A, B, D and E. There was no significant (p > 0.05) variation in mean

serum albumin, globulin and creatinine levels among the groups throughout the period of

study. The serum copper concentration was significantly (p < 0.05) lower in the naturally

infested groups A, B and C when compared to in-contact group D and control group E. There

were no significant (p > 0.05) differences in the serum vitamin A and zinc levels between the

groups although their levels were lower in naturally infested groups A, B, and C when

compared to groups D and E. Although serum cortisol and testosterone concentrations were

lower in the naturally infested groups A, B and C when compared to the in-contact group D

and control group E, the differences were not statistically significant (p > 0.05). The mean

testicular and epididymal sperm reserves decreased significantly (p < 0.05) in all the

Sarcoptes scabiei-infested groups A, B, C and D when compared to the control group E. Skin

section of infested goats showed variable degrees of acanthosis, hyperkeratosis, parakeratosis

and intracorneal pustules while the dermis had variable degrees of cellular infiltrate

(neutrophils, eosinophils, lymphocytes) and fibroblast proliferation.

ix

This study has established that sarcoptic mange in WAD goat led to decreased red

blood cell counts, haemoglobin, packed cell volume (anaemia) but increased total white

blood cell counts, neutrophils and lymphocytes. Serum biochemistry also indicated decreased

total serum protein, albumin, copper, zinc, and vitamin A levels but increased creatinine. The

most striking feature of the disease in WAD goats was the decreased testosterone levels and

spermatogenesis. Histopathologic investigations showed that sarcoptic mange was associated

with non-specific skin reactions such as parakeratosis, hyperkeratosis, acanthosis but most

importantly epidermal pustules with varying degrees of dermal/epidermal cellular infiltration

(neutrophils, eosinophils, lymphocytes) and dermal fibrosis.

x

TABLE OF CONTENTS

Title page - - - - - - - - i

Declaration - - - - - - - - iii

Certification - - - - - - - - iv

Dedication - - - - - - - - v

Acknowledgement - - - - - - - vi

Abstract - - - - - - - - vii

Table of contents - - - - - - - x

List of tables - - - - - - - - xv

List of figures - - - - - - - - xvii

CHAPTER ONE INTRODUCTION - - - - 1

1.1 Introduction - - - - - - - 1

1.2 Objectives of the study - - - - - - 3

CHAPTER TWO: LITERATURE REVIEW - - - 4

2.1The West African Dwarf Goats - - - - - 4

2.2 Mange - - - - - - - - 5

2.3 Sarcoptic mange - - - - - - - 5

2.4 Psoroptic,Chorioptic and Demodectic mange in goats - - 6

2.5 Etiology of sarcoptic mange - - - - - 8

2.6 Morphology of Sarcoptes scabiei - - - - - 8

2.7 Hosts - - - - - - - - 10

2.8 Transmission of Sarcoptes scabiei - - - - 11

2.9 Life cycle and epidemiology of Sarcoptes scabiei - - 11

2.10 Pathogenesis - - - - - - - 12

2.11 Clinical signs and features- - - - - 13

2.12 Host immune response - - - - - - 13

2.13 Pathology - - - - - - - 15

2.14 Diagnostic techniques - - - - - - 15

2.14.1 Clinical diagnosis - - - - - - 15

2.14.2 Light microscopy - - - - - - 16

xi

2.24.3 Therapeutic diagnosis- - - - - - 17

2.14.4 Dermatoscopy - - - - - - - 17

2.14.5 Antigen detection and PCR technique - - - - 18

2.14.6 Intradermal skin test for scabies - - - - 18

2.14.7 Antibody detection - - - - - - 18

2.15 Therapeutic management of sarcoptic mange - - - 18

2.16 Control and prevention - - - - - - 19

CHAPTER THREE: MATERIALS AND METHODS - - 20

3.1 Experimental animals and housing - - - - 20

3.2 Feeding - - - - - - - - 21

3.3 Experimental Design - - - - - - 21

3.4 Parasitological Examination - - - - - 21

3.5 Source of mite for in- contact transmission - - - 22

3.6 Clinical monitoring of in-contact transmission experiment - 22

3.7 Sample Collection - - - - - - 22

3.8 Haematological studies - - - - - - 23

3.7.4 Packed cell volume - - - - - - 23

3.7.5 Hemoglobin concentration - - - - - 23

3.7.6 Erythrocyte counts - - - - - - 23

3.7.7 Erythrocytic indices - - - - - - 24

3.7.7A Mean corpuscular volume - - - - - 24

3.7.7B Mean corpuscular hemoglobin - - - - 24

3.7.7C Mean corpuscular hemoglobin concentration - - - 24

3.7.8 Total leucocyte count - - - - - - 25

3.7.9 Differential leucocyte counts - - - - - 25

3.8 Determination of serum total protein - - - - 26

3.8.2 Procedure - - - - - - - 26

3.9 Determination of serum albumin - - - - - 27

3.9.2 Procedure - - - - - - - 27

3.10 Determination of serum creatinine - - - - 27

3.10.2 Procedure - - - - - - - 27

3.11 Determination of serum vitamin A - - - - 28

xii

3.11.2 Procedure - - - - - - - 28

3.12 Determination of serum zinc and copper - - - 2

3.12.2 Procedure - - - - - - - 29

3.13 Adrenal and gonadal steroid concentration - - - 29

3.13A Determination of serum testosterone - - - - 29

3.13B Procedure - - - - - - - 29

3.13C Determination of serum cortisol - - - - 30

3.13D Procedure - - - - - - - 30

3.14 Determination of gonadal and extra-gonadal sperm reserves - 31

3.14.2 Procedure - - - - - - - 31

3.14.2A Epididymal sperm reserve - - - - - 31

3.14.2B Testicular sperm reserve - - - - - 31

3.15 Histopathology - - - - - - - 32

3.15.2 Procedure - - - - - - - 32

3.16 Data Analysis - - - - - - - 32

CHAPTER FOUR: RESULTS - - - - - 33

4.1 Parasitological examinations - - - - - 33

4.2 Clinical evaluation of experimentally exposed goats - - 35

4.3 Haematology - - - - - - - 40

4.3.1 Packed cell volume - - - - - - 40

4.3.2 Haemoglobin concentraton - - - - - 41

4.3.3 Erythrocyte count - - - - - - 42

4.3.4 Erythrocytic indices - - - - - - 43

4.3.4A Mean corpuscular volume - - - - - 43

4.3.4B Mean corpuscular hemoglobin - - - - 44

4.3.4C Mean corpuscular hemoglobin concentration - - - 45

4.3.5 Total leucocyte count - - - - - - 46

4.3.6 Differential leucocyte counts - - - - - 47

4.3.6A Absolute neutrophil count - - - - - 47

4.3.6B Absolute lymphocyte counts - - - - - 48

4.3.6C Absolute monocyte counts - - - - - 49

4.3.6D Absolute eosinophil counts - - - - - 50

4.3.6E Absolute basophil counts - - - - - 51

xiii

4.4 Gonadal and extragonadal sperm reserve - - - 52

4.4.1 Caput epididymal sperm reserve - - - - 52

4.4.2 Corpus epididymal sperm reserve - - - - 53

4.4.3 Cauda epididymal sperm reserve - - - - 54

4.4.4 Total epididymal sperm reserve - - - - - 55

4.4.5 Right testicular sperm reserve - - - - - 56

4.4.6 Left testicular sperm reserve - - - - - 57

4.4.7 Combined testicular sperm reserve - - - - 58

4.5 Serum biochemical assay - - - - - 59

4.5.1 Serum vitamin A, zinc and copper concentrations - - 60

4.5.2 Gonadal and Adrenal steroid concentrations - - - 61

4.6 Histopathology - - - - - - - 62

CHAPTER FIVE: DISCUSSION AND CONCLUSION - - 71

5.1 Discussions - - - - - - - 71

5.2 Conclusions - - - - - - - 75

REFERENCES - - - - - 76

xiv

LIST OF TABLES

Table1: Chronology of the appearance of clinical manifestations in the experimentally

exposed WAD goats of group E.

Table 2: Mean (±SEM) Packed Cell Volume of the naturally infested groups (A, B, C),

exposed group D and control WAD goats group E .

Table 3: Mean (±SEM) Haemoglobin Concentratio of the experimental groups A, B, C, D

and the control E .

Table 4: Mean (±SEM) Erythrocyte count of the experimental groups A, B, C, D and the

control group E.

Table 5: Mean (±SEM) Corpuscular Volume of the experimental groups A, B, C, D and

control groups E goats.

Table 6: Mean (±SEM) corpuscular Haemoglobin of the infested groups A, B, C, D and

control group E.

Table 7: Mean (±SEM) Corpuscular Haemoglobin Concentrations of the experimental

groups A, B, C, D and control group E WAD goats.

Table 8: Mean (±SEM) Total Leukocyte counts of the experimental groups A, B, C, D and

control group E WAD goats.

Table 9: Mean (±SEM) Absolute Neutrophil count of the experimental groups A, B, C, D

and control group E WAD goats.

Table 10: Mean (±SEM) Absolute Lymphocyte count of the experimental groups A, B, C, D

and control group E WAD goat.

Table 11: Mean (±SEM) Absolute Monocyte count of the experimental groups A, B, C, D

and control group E WAD goats.

Table 12: Mean (±SEM) Absolute Eosinophil count of the naturally infested groups A, B, C,

exposed group D and control group E.

Table 13: Mean (±SEM) Absolute Basophil count of the experimental groups A, B, C, D and

control group E.

Table 14: Mean (±SEM) Serum Biochemical changes of the experimental groups A, B, C, D

and control group E.

Table 15: Mean (±SEM) Serum Vitamin A, Zinc and Copper concentrations of the

experimental groups A, B, C, D and control group E.

xv

Table 16: Mean (±SEM) Serum Testosterone and Cortisol concentrations of the experimental

groups A, B, C, D and control group E.

Table.17. Summary of histological lesions in the experimental groups A, B, C, D and control

group E.

xvi

LIST OF FIGURES

Figure 1: A picture of adult Sarcoptes scabiei. Courtesy of S.J. Upton, Kansas State

University and Thomas Nolan, University of Pennsylvania.

Figure 2: Pictures of other mites (left to right) Psoroptic ear mite (Psoroptes cuniculi),

chorioptic scab mite (Chorioptes bovis) and goat follicle mite, (Demodex caprae)

Figure 3: Sarcoptes scabiei mite isolated from the infested goats, identified by its round

shape and short legs (10% potassium hydroxide preparation, x400 magnification)

Figure 4: Photomicrograph of an un hatched egg of Sarcoptes scabiei containing a larvae

(10% potassium hydroxide preparation, x400 magnification)

Figure 5: A picture of experimentally exposed goat showing lesions around the ears.

Figure 6: A picture of experimentally exposed goat showing lesions around the eyes.

Figure 7: A picture of experimentally exposed goat showing lesions around the ears and

eyes.

Figure 8: Mean (±SEM) Caput Epididynal Sperm Reserve of infested groups A, B, C, D and

control group E WAD goats.

Figure 9: Mean (±SEM) Corpus Epididymal Sperm Reserve count sperm reserve of infested

groups A, B, C, D and control group E WAD goats.

Figure 10: Mean (±SEM) Cauda Epididymal Sperm Reserve count of the naturally infected

group A (mild), B (moderate), C (severe infestation), in contact group D and control

group E WAD goats.

Figure 11: Mean (±SEM) Total Epididymal Sperm Reserve of naturally infected WAD goats

group A, B, C, in contact group D and control E. WAD goats

Figure 12: Mean (±SEM) Right Testicular Sperm Reserve count of naturally infected groups

A, B, C, in-contact group D and the control E.

Figure 13: Mean (±SEM) Left Testicular Sperm Reserve of infested groups A, B, C, D and

control group E WAD goats.

Figure 14: Mean (±SEM) Combined Testicular Sperm Reserve of infested groups A, B, C, D

and control group E WAD goats.

Figure 15: Photomicrograph of skin section from group E (control) goats showing normal

epidermis (black arrow), the dermis (D) and hair follicles (white arrow). H and E x 100.

Figure.16: Photomicrograph of a skin section from group A (mildly infested) goats showing

hyperkeratosis (H) and epidermal pustules (EP).H and E x 400.

xvii

Figure 17: Photomicrograph of skin section from group B (moderately infested) goats

showing degenerating section of the mite (black arrow), pustule (P), rete peg formation

(white arrow) and mononuclear cells infiltration of the papillary dermis (PD) .H and E x 100.

Figure 18: Photomicrograph of skin section from group B (moderately infected) goats

showing epidermal pustules (black arrow) and hyperplasia (white arrow).H and E x 400.

Figure 19: Photomicrograph of skin section from group C (severely infested) goats showing

a section of the parasite (black arrow), hyperplasic epidermis (H), severe mononuclear

cellular infiltration of the dermis (PD) and intracorneal pustules (white arrow). H and E x

100.

Figure 20: Photomicrograph of skin section from group C (severely infested) goats showing

intense granulation tissue formation (DF). Note the sloughed off epidermal area (arrow). H

and E x 100.

Figure 21: Photomicrograph of skin section from group D (in contact) goats showing

vacuolation of keratinocytes (black arrows) and epidermal parakeratosis (white arrow). H and

E x 400.

1

CHAPTER ONE

INTRODUCTION

1.1 Introduction

The rapid changing pattern of demand for livestock and livestock products

emphasizes the importance of the livestock subsector to the agricultural economy of Nigeria.

Within the small ruminant husbandry, goat rearing plays an important role in the socio-

economic life of the rural people in a developing country like Nigeria. In southern Nigeria,

the West African Dwarf goat is the most predominant small ruminant reared and over 70% of

the rural community keeps them (ILCA, 1987; Olubunmi, 1995). They are often termed the

“poor man’s cow’’. Their small size permit them to be maintained on a limited area and they

consume a wide variety of grasses, weeds, shrubs, tree leaves and crop residues that

otherwise go waste and cause pollution (Kumar et al., 2010). Goat meat (Chevon) is

preferred over other meats because it is leaner and suffers no religious taboos. Thus, in

Nigeria, goats are kept for meat, as a source of cash income and manure among other socio-

economic, religious and cultural reasons (Olubumni, 1995; Adeloye, 1998; Ujjwal and Dey,

2010). In addition to the ability of the West African Dwarf goats to live and reproduce in

harsh environmental conditions kidding twins and triplets, they are also valued as insurance

or investment against crop failure (Devendra, 1976, Adeloye, 1998; ILRI, 1999; Jajasuriya,

1999; Minjauw and McLeod, 2003).

Disease problems in the small ruminants remains the major hurdle to the realization of

the full potential of goat production for better economic return and research in the livestock

industry, which need timely and effective intervention in management. (Francis, 1988;

Kumar, et al., 2010). Infectious and non-infectious diseases influence the economic

production of goats. Endo- and ectoparasitic diseases constitute a very important problem.

From within the ectoparasites, the mite Sarcoptes scabiei imposes major economic and health

threat to the production of West African Dwarf goats in southern Nigeria (Francis, 1988;

Olubunmi, 1995; Okewole, 1997; Shoyinka et al., 2009). The infestation by this mite

2

popularly called sarcoptic mange, scabies or sarcoptidosis is a parasitic skin disease that has

been described in more than 100 species of mammals including man (Ibrahim and Abu-

Samra, 1987; Scott, 1988; Bornstein et al., 2001).It is known to be the most common,

stubborn, unpleasant and difficult to treat of all mange infestations in the goat and there is

now documented reports of its resistance to commonly known therapeutic drugs such as the

avermectins (Jackson et al., 1983; Manurung et al., 1990; Smith and Sherman, 1994;

Okewole, 1997; Currie et al., 2004; Shoyinka et al., 2009). The disease is characterized by

intense pruritus, dermatitis, alopecia, emaciation, weakness, anorexia, very high morbidity

and mortality in domestic and farm animals (Amsalu et al., 2000; Walton et al., 2004;

Giadinis et al., 2011). The mite inflicts severe damage to the hosts’ skin by forming tunnels

within the upper epidermal layers (Morris and Dunstan, 1996) and transmission is believed to

be by direct contact with infested domestic or wild animals, formites, pasture and flies (Kral

and Schwartanan, 1964; Andrews, 1983; Jackson et al., 1983; Anderson et al., 2002; Curtis,

2004). Although, epidemiological studies on Sarcoptic mange of goats in Nigeria reported

prevalence rates of 17.27% and 15.66% in affected areas of southwestern and southeastern

Nigeria respectively (Olubunmi, 1995; Shoyinka et al., 2009), mortality rates of 57% to 60%

have been reported in some flock from different parts of the world (Amsalu et al., 2000;

Nektarios et al., 2011).

Despite the economic and health importance of Sarcoptes scabiei infestation in both

animal and human population, the pathogenicity, pathogenesis and pathology of the disease is

poorly understood (Bornstein and Zakrisson 1993, Skerrat et al., 1999; Rambozzi et al.,

2007). For instance, some studies reported that the lesions of Sarcoptes scabiei infestation are

not limited to the skin alone and includes lymphoid hyperplasia, generalized

lymphoadenopathy, hepatic and renal amyloidosis, hypothyroidism, bronchopneumonia as

well as gonadal degeneration in both domestic and wild animals (Anderson, 1981; Folz,

1984; Arlian et al., 1990; Little et al., 1998; Skerrat et al., 1999; Nakagawa et al., 2009).

These extra dermal lesions are thought to be due to the adverse effects of pro-inflammatory

cytokines or secretion of some toxins by mites that affects the vital organs. However, the role

of the highly reactive oxygen species (ROS) in the pathogenesis of ectoparasitic disease has

become an area of hot debates in recent years, as excess free radical generation due to

Sarcoptes scabiei infestation have been reported in goats and dogs (Camkerten et al., 2009;

Ujjwal and Dey, 2010) It is speculated that the combined effects of these free radicals and

3

products of mite activity may be associated with organs dysfunction in scabies-infested

animals (Ujjwal and Dey, 2010).

Available reports on the clinicopathology of sarcoptic mange in rabbits, dogs, foxes,

sheep, camels, goats, pigs, coyotes and wild raccoon are inconsistent (Sheahan, 1975; Arlian

et al., 1988a,1995; Dalapati et al., 1996; Gorakh et al., 2000; Parmar et al., 2005; Hafeez et

al., 2007; Shoyinka et al., 2009). Such inconsistencies are most probably the result of host

differences or severity of disease.

However, the tendency by previous workers to ignore the fact that the degree of

severity is most likely to be directly related to the degree of systemic involvement in

sarcoptic mange, adds to the difficulty of comparing the results of available and probably

conflicting reports. It is therefore necessary to have a better understanding of the

pathophysiology of Sarcoptes scabiei infestations of goats using hematologic, biochemical

and morphologic parameters based on the severity of clinical disease.

1.2 OBJECTIVES OF THE STUDY

1. To establish experimental contact transmission of sarcoptic mange to susceptible WAD

goat.

2. To evaluate the effects of sarcoptic mange on the hematologic and some biochemical

indices (including trace minerals and vitamin A) of WAD goat.

3. To assess the effects of sarcoptic mange on spermatogenesis (gonadal and extra-

gonadal sperm reserves), adrenal cortisol and gonadal hormone concentrationin WAD goat.

4. To document the histomorphologic changes in the skin sections of natural and

experimental Sarcoptes scabiei-infested WAD goat.

4

CHAPTER TWO

LITERATURE REVIEW

2.1 THE WEST AFRICAN DWARF GOATS

Goats are small ruminants that belong to the Family Caprini. It is the earliest

domesticated animal. They are distributed worldwide but 74% of the world populations of

goats are reared in the tropical and subtropical countries (Devendra and Burns, 1983). The

West Africa Dwarf (WAD) goats are mainly found in the region of latitude 14oN across West

Africa in the coastal area, where they thrive well and reproduce with twins and triplets in the

ecological niche (Adeloye, 1998). In Nigeria and in West Africa, the West African Dwarf

goats are reared traditionally at subsistence level where they are allowed to scavenge and care

for their own nourishment (Adeloye, 1985).

In this region, they contribute significantly to the agricultural economy especially to

the landless peasants and small holder farmers (ILCA, 1987). Following scavenging and

browsing by the day, the WAD goats are sometimes kept in paddocks and sheds at night so

that their droppings are used as manure for enhancing crop yield since availability of

fertilizers are limited (Devendra and Burns, 1983). They are also kept for meat and skin in

addition to the income they generate when sold (Olubunmi, 1995).The WAD goats are also

used mainly for traditional ceremonies, celebration of festivals and performance of religious

rites in the region.

The major threats to improved goat production in Nigeria in particular and West

Africa in general are health problems such as Peste des Petits Ruminants (PPR), Contagious

Pustular Dermatitis, Foot rot, Reproductive disorders (dystocia & abortions) and Mange

(Francis, 1988). Hence, it is necessary to increase research on these diseases to attain

improved productivity in the WAD goats.

5

2.2 MANGE

Mange is an important skin disorder that affects all animals such as dogs, cats and

goats (Terry, 2011, Nwoha, 2011). Mange affects all warm blooded animals and it is caused

by different mites which tunnel within the skin of infected animals to suck blood and lymph,

thereby causing ulcers and scabs which predispose the infested animals to infection that

spread rapidly without proper treatment and prevention (Lughano and Dominic, 2006; Terry,

2011). Goats are particularly infected by four types of mites, each morphologically distinct

from the other but with overlapping clinical presentations. They include those causing

Psoroptic, Chorioptic, Demodectic and Sarcoptic mange (Radostits et al., 2000).

2.3 SARCOPTIC MANGE

Sarcoptic mange or scabies is a highly contagious and pruritic acariosis (of the skin)

affecting more than 100 domestic and wild mammalian species including man (Ibrahim and

Abu-samra, 1987; Scott, 1988; Bornstein et al., 2001). The disease is reported to affect

mainly the traditional goat herds with newly purchased animals known to be the source of

contamination (Jackson et al., 1983; Scott, 1988; Anderson et al., 2002). The disease has

been described as a dreadful disease especially in the tropics (Soulsby, 1998). This form of

mange in goats is worldwide in distribution but it is of greatest economic importance in areas

where goats are the basic domestic ruminants kept. The condition is usually chronic

(Urquhart et al., 1996).

6

2.4 PSOROPTIC, CHORIOPTIC AND DEMODECTIC MANGE IN GOATS

Goats can be infested by several other species of mites, such as goat follicle mite

(Demodex caprae), , psoroptic ear mite (Psoroptes cuniculi), and chorioptic scab mite

(Chorioptes bovis). See figure 1 below. The goat follicle mite causes dermal papules and

nodules and this resulting condition is known as demodectic mange in goats. These papules

or nodules are caused by hair follicles or gland ducts becoming obstructed and producing

these swellings, trapping the mites within these lesions. These continue to enlarge as the

mites multiply, sometimes reaching several thousand mites per lesion. Cases of demodectic

mange occur most commonly in young animals, pregnant does, and dairy goats. Papules

usually appear on the face, neck, axillary region, or udder and these papules can enlarge to 4

cm in diameter as mites multiply. Nodules can rupture and exude the mites, resulting in

transmission of the mite to other animals. Transmission of the goat follicle mite to newborn

goats typically occurs within the first day following birth. Other possible means of transfer

are licking and close contact during mingling or mating (Soulsby, 1998; Tally and Sparks,

2012).

The psoroptic ear mite or ear mange mite causes lesions on or in the ear of the host

animal. These lesions cause crust formation, foul odor discharges in the external ear canal,

and behavioral responses such as scratching the ears, head shaking, loss of equilibrium, and

spasmodic contractions of neck muscles. Psoroptic ear mite lives its entire life under the

margins of scabs formed at infested sites. There the eggs are deposited and hatch in 4 days.

The complete life cycle takes about 3 weeks. All stages of this nonburrowing mite pierce the

outer skin layer. Transmission of this mite occurs between animals by direct contact. Goats

usually less than 1 year old generally exhibit higher infestation rates than do older animals.

Signs of the psoroptic ear mite in kids are often observed as early as 3 weeks after birth,

reflecting transfer of mites from mother to young. By 6 weeks of age, most kids in infested

7

goat herds are likely to harbor these mites. Chronic infestations have lead to anemia and

weight loss in goats (Soulsby, 1998)

The chorioptic scab mite causes chorioptic mange in domestic animals, especially in

cattle, sheep, goats, and horses. This mite occurs primarily on the legs and feet of its hosts,

where all of the developmental stages are likely to be found. Eggs are deposited singly at the

rate of one egg per day and are attached with a sticky substance to the host skin. Adult

females usually live for 2 weeks or more, producing about 14-20 eggs during this time. Eggs

hatch in 4 days and are often clustered as multiple females lay their eggs in common sites.

The immature stages last anywhere from 11 to 14 days and the entire life cycle is completed

in 3 weeks. Infestations of chorioptic scab mite tend to be higher in goats than in sheep, with

up to 80 to 90 percent of goats in individual herds being parasitized. The mites occur most

commonly on the forefeet of goats, where the largest numbers of mites and lesions are

usually associated with the accessory claws. However, they also can occur higher on the foot

(Tally and Sparks, 2012).

2.5 AETIOLOGY OF SARCOPTIC MANGE

The cause of sarcoptic mange is the mite Sarcoptes scabiei of the Family: Sarcoptidae

and Genus: Sarcoptes. The specie is believed to have a number of sub species or varieties

which are host specific and thus designated as Sarcoptes scabiei var bovis, Sarcoptes scabiei

var ovis and Sarcoptes scabiei var capri for cattle, sheep and goats respectively (Radostits et

al, 2000). The mange mite Sarcoptes scabiei was first identified and described by Aristotle

(384 to 322 BC) as “lice in the flesh” and utilizing the term “akari”. Subsequently, scabies

was mentioned by many writers, including the Arabic physician Abuel Hassan Ahmed el

Tabari, around 970BC, Saint Hildegard (1098 to 1179), and the Moorish physician Avenzoar

(1091 to 1162) (Ramos-e-Silva, 1998). In 1687, Bonomo and Cestoni accurately described

8

the causes of scabies in a report (Montesu and Cottoni, 1991). Their description recounting

the parasitic nature, transmission, possible cures and microscopic drawings of the mite and

eggs of Sarcoptes scabiei is believed to be the first mention of the parasitic theory of

infectious diseases. Nevertheless, it was not until 1868, two centuries later, that the cause of

scabies was established with the publication of a treatise by Hebra (Burgess, 1994).

2.6 MORPHOLOGY OF SARCOPTES SCABIEI

Sarcoptes scabiei is a creamy white microscopic parasite which is roughly circular

in outline.The female measures up to 330-600µm by 250 – 400µm and the male 200 -

400µm by 150 - 200µm. Thus, the male is smaller than the female. Larvae has six legs,

while nymphs and adults have eight legs, with stalked puvilli (suckers) present on legs 1 and

2 of both the male and female adult mites, enabling them to grip the substrate. Additionally,

mites bear spur – like claws, and they have six or seven pairs of spine – like projections on

their dorsal surfaces.

The adult male is distinguishable from the female by its smaller size, darker colour

and the presence of stalked puvilli on leg 4 while leg 4 in the adult female ends in a long

setae (Soulsby, 1998; Walton and Currie, 2007).

9

Figure 1. A picture of adult Sarcoptes scabiei. Courtesy of S.J. Upton, Kansas State

University and Thomas Nolan, University of Pennsylvania.

10

Figure 2. Pictures of other mites (left to right): Psoroptic ear mite (Psoroptes cuniculi),

chorioptic scab mite (Chorioptes bovis) and goat follicle mite, (Demodex caprae), Credits:

S.J. Upton, Kansas State University and Thomas Nolan, University of Pennsylvania.

11

2.7 HOSTS

Sarcoptic mange affects human, domestic animals and wildlife populations (Gross et

al., 1992; Pence and Ueckermann, 2002; Walton and Currie, 2007). The Sarcoptes scabiei

mite was known to be originally a parasite of primates that spread to domestic animals and

eventually to wild animals. Such spread was said to be influenced by ecological factors such

as deforestation and intrusion of people and domestic animals into the traditional habitat of

wildlife populations (Nakagawa et al., 2009).

Mite populations are primarily host specific, with little evidence of interbreeding

between strains. Cross-infection studies describe unsuccessful experimental attempts to

transfer scabies mites from dogs to mice, pigs, cattle, goats, and sheep (Arlian et al., 1984a).

This was supported by molecular genotyping studies that reveal genetically distinct dog and

human host associated mite populations in Australian indigenous communities where scabies

is endemic (Walton et al., 1999; Walton et al., 2004). Occasional cases of human scabies

have been reported following exposure to animal scabies, but were said to be self-limiting,

with no evidence of long-term reproduction occurring on the non-normal host (Beck, 1965).

Despite the above studies, it is still not clear whether the mites taken from different

hosts constitute different species or whether they are just varieties of a single species (Arlian,

1989). However, the consensus of opinion up to now has been that it is single species with

the ability to vary and adapt. Although, it is not known to what extent, cross-infection does

actually occur between some hosts (Arlian, 1989).

12

2.8 TRANSMISSION OF SARCOPTES SCABIEI

Sarcoptes scabiei transmission is mediated primarily by close, prolonged physical

contact with infected animal (Kral and Schwartzman, 1964). Also, rubbing against formites

or pasture to relieve the pruritus induced by the mite contributes to the transmission of the

disease in the herd (Yeruham et al., 1996). High density of animal populations also

facilitates transmission. All life stages of Sarcoptes scabiei may survive in the host’s

environment for days and even weeks, depending on the relative humidity and temperature

(Arlian et al., 1989). Gerasim off (1953), cited in Andrews, (1983) claimed that even

transmission of sarcoptic mites by flies is possible.

When mites are dislodged from their host, they can survive for 24 to 36 hours at room

temperature with normal humidity (210C and 40 to 80% relative humidity) and even longer at

lower temperatures with high humidity (Arlian et al., 1984a). However, the mites’ ability to

infest the host decreased with increased time off the host. The sightless mite uses odor and

thermal stimuli for active host taxis (Arlian et al., 1984b; Arlian et al., 1988b).

2.9 LIFE CYCLE AND EPIDEMIOLOGY OF SARCOPTES SCABIEI

According to Urquhart et al (1996), the fertilized female creates a winding burrow or

tunnel in the upper layers of the epidermis, feeding on lymph and epidermal tissues. The

eggs are laid in those tunnels and hatch in 3 – 5 days, and the six-legged larvae crawl unto the

skin surface. These larvae in turn burrow into the superficial layers of the skin to create

“moulting pockets” in which their moult to nymph and adult are completed. The male

emerges to seek a female either on the skin surface or in a moulting pocket. The male mite is

reported to die after mating, although this has been disputed (Heilesen, 1946; Alexander,

1984). After fertilization, the females produce new tunnels. The entire life cycle is completed

in 17 – 21 days. The mites are transmitted chiefly by direct contact between hosts. All the

13

developmental stages of the life cycle (larvae, nymph and adult) are capable of migration.

Formites also serve as carriers (Radostits et al., 2000). The adults are usually susceptible to

dryness and do not survive for more than few days off their host, though under optimal

laboratory conditions, mites may live for three weeks (Soulsby, 1998). Studies have shown

that animals in poor body condition appear to be most susceptible to Sarcoptes scabiei

infection. Also overcrowding, poor nutrition, poor husbandry and general mismanagement

predisposes animals to mange (Okewole, 1997; Radostits et al., 2000). Mange is known to

be most active in the rainy season but improve slightly during the dry season (Chineme et al.,

1979; Olubunmi, 1995; Soulsby, 1998).

2.10 PATHOGENESIS OF SARCOPTIC MANGE.

According to Soulsby (1998) the parasite Sarcoptes scabiei pierces the skin of the

host to suck lymph and may also feed on young epidermal cells. Their activities produce a

marked irritation which causes intense itching and scratching. The resulting inflammation of

the skin is accompanied by exudates which coagulates and forms crusts on the surface. This

is further characterized by excessive keratinization, proliferation of connective tissue which

results in thickened and wrinkled skin. There is concomitant loss of hairs which may be

widespread. The intense pruitus caused by the activities of those mites leads to excoriations

and secondary bacterial infections of the skin. In untreated cases, systemic effects such as

anorexia, emaciation, weakness and death may occur (Dorny et al., 1994; Radostits et al.,

2000; Leon-Vizcaino et al., 2001; Rehbein et al., 2003; Nektarios et al., 2011).

14

2.11 CLINICAL SIGNS/FEATURES OF SARCOPTIC MANGE.

In small ruminants, clinical presentation of primary infection with Sarcoptes scabiei

is reported to take place in 4 to 6 weeks after infection (Kambarage, 1992). Presentation is

with generalized itching, which is frequently reported to be more intense at night. The intense

irritation caused by the activities of the mite leads to the rubbing of the animal on hard

surfaces resulting in partial or complete alopecia. The alopecia is evident on the medial

aspect of the hindlimbs, axillae, brisket, abdomen, trunk, udder and teats (Kambarage, 1992;

Olubunmi, 1995) There is appearances of dry and bran-like scales on the face, around the

nostrils and ears which later become hard crusts extending from the muzzle to the area

between the eyes and nostrils, region between the eyes and horn, inner and outer parts of the

ears. The skin then becomes thickened and wrinkled with cracks and fissures on the hock

joint, scrotum and pinnae with heavy dandruff evident on hairy areas covering the neck and

abdominal regions (Chineme et al., 1979; Kambarage, 1992; Olubunmi, 1995; Karin, 2005;

Lughano and Dominic, 2006; Merck’s, 2011; Nwoha, 2011).

2.12 HOST IMMUNE RESPONSE

Although published data on the immunologic responses of goats to scabies is limited

or non-existent, considerable studies have been done on other species. Despite the fact that

the mite resides in dead skin tissue, mite antigens enter the lower epidermal and dermal skin

layers and induce both a circulating antibody and a cell-mediated immune response in the

vicinity of the scabietic lesion (Hancock and Milford-Ward, 1974; Fernandez et al., 1977;

Falk, 1980, 1981; Falk and Bolle, 1980 a, b; Hoefling and Schroeter, 1980; Chevrant-Breton

et al., 1981; Falk and Eide, 1981; Rantanen et al., 1981; Van Neste and Lachapelle, 1981;

Falk and Matre, 1982; Reunala et al., 1984; Van Neste and Staquet, 1986; Van Neste, 1987;

Morsy and Gaafar, 1989; Cabrera et al., 1993; Arlian et al., 1994 a, b; Lastras et al., 2000).

15

Thus, studies of the symptoms and signs of scabies point to the development of host

immunity but until the scabies Gene Discovery Project (Fischer et al., 2003), only a small

number of the antigens responsible for the immune reactions to scabies had been sequenced

and characterized ( Mattsson et al., 2001; Harumal et al., 2003). However, there is still dearth

of literature reporting scabies specific humoral or cellular immunity. Limited past

investigations of humoral immunity in scabietic patients show contradictory results and have

used whole-mite scabietic extracts from other hosts, such as dogs (Morgan et al., 1997).

Immunoblotting studies demonstrate that sera from crusted scabies patients showed strong

IgE binding to over 21 S. scabiei var canis proteins (Arlian et al., 2004). However, the

identity of these allergens was unknown but patients with scabies are known to have

extremely high serum levels of IgE and IgG (Roberts et al., 2005).

Cell mediated host immune responses have been identified primarily by

histopathological examination of skin biopsy specimens from mange lesions. Mite burrows

were found to be surrounded by inflammatory cell infiltrates comprising lymphocytes,

neutrophils, eosinophils, plasma cells, mast cells, macrophages and other mononuclear cells

in rabbits, pigs, humans, and wombats (Hejazi and Mehregan, 1975; Sheahan, 1975;

Fernandez et al., 1977; Falk and Eide, 1981; Van Neste and Lachapelle, 1981; Falk and

Matre, 1982; Reunala et al., 1984; Morsy and Gaafar, 1984 ;Van Neste and Staquet 1986;

Van Neste, 1987; Arlian et al., 1994b; Skerrat, 2003).

Although, experimental studies showed that dogs previously infested with S. scabiei

var canis developed protective immunity to subsequent parasite challenge, the mechanism of

such resistance is not known (Arlian et al., 1996). This was also reported by Mellanby,

(1944) that scabietic patients were resistant to subsequent reinfestation just as immunization

with extracts of house dust mites (D. farinae and D. pteronyssius) containing antigens that

16

cross react with S. scabiei var canis induced protective immunity in 71% of vaccinated hosts

(Arlian et al., 1995).

2.13 PATHOLOGY

The common gross skin lesions usually associated with mange in domestic animals

include patches of erythema, alopecia, scaling and crusts (Thomson, 1988). According to

Kambarage (1992) characteristic skin lesions of sarcoptic mange in goat include crusty and

alopecic patches on the muzzle, neck region, scrotum, medial aspect of thigh and the hock

region or sometimes extending to the whole of scrotal-thigh-hock region. He also observed

that cracks and fissures were evident among lesions at the hock joint and that there is usually

a high degree of thickening and wrinkling of skin in the affected areas. Besides, the crusty

and alopecic areas, heavy dandruff was evident in hairy areas where there was little evidence

of alopecia and crusty materials.

Histologically, there is epidermal hyperplasia with marked hyperkeratosis,

perivascular leucocytic infiltration, hyperemia and edema with foci of epidermal necrosis in

sarcoptic mange (Thomson, 1988). There are reports of histological examination of skin

biopsy from affected animals that revealed adult mites and their eggs buried deep in the

epidermis especially at the Malpighian and granulosum layers (Chineme et al., 1979; Darzi et

al., 2007).

2.14 DIAGNOSTIC TECHNIQUES

2.14.1 Clinical Diagnosis

Currently, there is no efficient means of diagnosing animal or human scabies. To

date, diagnosis is through clinical signs and microscopic examination of skin scrapings, but

experience has shown that the sensitivity of these traditional tests is less than 50% (Walton

and Currie, 2007).Visible lesions are not characteristic as they are often obscured by eczema

or impetigo or are atypical. Detection of mite burrows with Indian ink was advocated more

17

than 20 years ago (Woodley and Saurat, 1981), but the test is often impractical hence not

used routinely. Presumptive diagnosis can be made on the basis of a typical history of

pruritus, the distribution of inflammatory papules, and a history of contact with other mange

cases (McCarthy et al., 2004). Most problematic is the situation with early and atypical cases

where gross skin lesions are either absent or exaggerated.

2.14.2 Light Microscopy

Definitive diagnosis of sarcoptic mange is based on the isolation and identification of

the mites, the eggs, eggshell fragments or mite fecal pellets from skin scrapings. One or two

drops of mineral oil are applied to the skin lesion, which is then scraped or shaved, and the

specimens examined after digestion in 10% KOH using a light microscope under low power.

This method provides excellent specificity but has low sensitivity for cases with low mite

burden (Walton and Currie, 2007). However, several factors may influence the level of

sensitivity. For example, the clinical presentation (unscratched lesions are more valuable),

the number of sites sampled and/or repeated scrapings, and the sampler’s experience. A skin

biopsy may confirm the diagnosis of scabies if a mite or parts of it can be demonstrated.

However, in most cases, the histological appearance is that of non-specific, delayed

hypersensivity reaction characterised by superficial and deep perivascular mononuclear cell

infiltrates with variable numbers of eosinophils, papillary edema, and epidermal spongiosis

(Chineme et al., 1979; Falk and Eide, 1981; Gorakh et al., 2000; Nakagawa et al., 2009).

In practice, identifying or demonstrating a mite is challenging, and a negative result,

even when done by an expert, does not rule out scabies. In the absence of confirmed mites,

diagnosis is currently based entirely on clinical and epidemiological findings. Due to the

extensive differential diagnosis, the specificity of clinical diagnosis is poor, especially for

18

those inexperienced with scabies. Also, there are difficulties in distinguishing among active

infestation, residual skin reaction and reinfestation (Walton and Currie, 2007).

2.14.3 Therapeutic Diagnosis.

Presumptive therapy can be used as a basis for diagnosis, but its value is questionable

and confounded by the variable delay until resolution of symptoms following therapy. A

positive response to treatment cannot exclude the spontaneous disappearance of a

dermatological disease other than scabies, and a negative response does not exclude scabies,

especially in resistant mites. (Chosidow, 2006; Walton and Currie, 2007).

2.14.4 Dermatoscopy.

A non-invasive technique that could be used in the diagnosis of scabies is the use of

epiluminescence microscopy and high resolution videodermatoscopy. This allows detailed

inspection of the patient’s skin from the surface to the superficial papillary dermis

(Argenziano et al., 1997; Haas and Sterry, 2001; Micali et al., 2004). Diagnosis is by

observation of a “jet with contrail” pattern in the skin representing a mite and its burrow.

This method is limited by the high cost of the equipment and requires expertise.

2.14.5 Antigen Detection and PCR Technique

A key weakness of PCR in scabies diagnosis is that it requires the presence of a mite

or its part in the sample. Thus it is unlikely to become a useful test in patients with low mite

burden. The method is also labour intensive and time consuming (Bezold et al., 2001).

2.14.6 Intradermal skin test for Scabies

The intradermal skin test for scabies is currently not feasible to use due to the inability

to culture sufficient quantities of Sarcoptes scabiei. Furthermore, whole mite extracts

obtained from animal models contain a heterogeneous mixture of host and parasite

19

antigens.However, purified, well characterized recombinant scabies mite allergens with

standardized protein contents could be of potential benefit in the future for scabies skin test

assays especially in cases clinically difficult to diagnose and for immunotherapy (Walton et

al.,2004).

2.14.7 Antibody Detection

Studies document that scabies mite infestation causes the production of measurable

antibodies in infested host species (Falk and Bolle, 1980a; Arlian et al., 2004). Also, host IgG

has been demonstrated in the anterior midgut and esophagus of fresh mites (Rapp et al.,

2006; Willis et al., 2006). Thus, ELISA techniques are now available for the detection of

antibodies to scabies in pigs and dogs (Bornstein et al., 1996; Bornstein and Wallgren. 1997;

Hollanders et al., 1997), but not in goats.

2.15 THERAPEUTIC MANAGEMENT OF SARCOPTIC MANGE

A number of drugs and medicaments have been used for the treatment of mange in

domestic animals. Some of these drugs are topically applied and examples include 0.3%

Coumphos, 0.15 – 0.25%, Phosmet, 0.03 – 0.1%, Diazinon, 2% Hot lime sulphur (Merck’s,

2011). In Nigeria, the common topical acaricides used are Diazinon, Benzyl Benzoate,

Asuntol® solution, used engine oil with 15% efficacy and sulphr oiltment with 25% efficacy

( Prashad, 1984; Olubummi, 1995).

Recently, Ivermectin, a macrocyclic lactone produced from Streptomyces avermitilis

has become the preferred drug of choice for the treatment of Sarcoptic mange and other mite

infestations in domestic animals. A single dose of 0.2mg/kg of the drug given parenterally

can control light infestation in goats but heavier infestations require a second dose at 10-14

days interval following the first injection (Radostits et al., 2000).

20

2.16 CONTROL AND PREVENTION

For effective control and prevention of sarcoptic mange in goat herds and other

domestic animals, the following steps have been recommended (Okewole, 1997).

- Vigorous treatment of all infested and in- contact animals.

- Disinfection of the environment with appropriate insecticide or the surrounding left for

at least 3 weeks before re-stocking.

- Culling of infected animals from the flock.

- Supportive nutrition

- Non-utilization of infected animals for breeding.

- Good hygiene in animal houses

21

CHAPTER THREE

MATERIALS AND METHODS

3.1 EXPERIMENTAL ANIMALS AND HOUSING

A total of twenty five (25) male West African Dwarf (WAD) goats between 8 and 12

months of age were divided into two groups of fifteen (15) naturally infested (Batch

A) goats with varying degrees of alopecia/dermatitis and 10 healthy (Batch B) goats

were used in this study.

Mite infestation was clearly demonstrated in Batch A goats before being selected for

the study while batch B goats were selected because they were free of mites and signs

associated with scabies.

The Batch A goats were procured from different households/livestock farms with

diagnosed outbreaks of sarcoptic mange, and sarcoptes scabiei demonstrated in their

skin scrapings. Such goats had varying degrees of itching, dermatitis, excoriation,

alopecia and crusts on affected areas of the body.

The Batch B goats were purchased from households/livestock farms that had no

clinical history of sarcoptic mange infestation over the previous one year. The two

groups of WAD goats were housed separately at the Experimental Animal House Unit

of the Department of Veterinary Pathology and Microbiology, University of Nigeria,

Nsukka.

The group B goats were acclimatized for two weeks during which they were

dewormed with levamisole hydrochloride and clinically evaluated to ensure that they

were free of cutaneous/systemic infectious/non-infectious disease conditions.

22

3.2 FEEDING

The animals were fed daily with freshly cut grasses tied in bundles and suspended in

each pen using a wire loop.

3.3 EXPERIMENTAL DESIGN

The fifteen (15) naturally infested WAD goats were purposively selected and assigned into

three (3) groups (A, B and C) of five (5) goats each, based on the degree of skin lesions while

the ten (10) healthy goats were randomly divided into two groups (D and E) of five (5) goats

each as follows:

Group A - (Mild-grade 1). Infested, with gross lesion affecting ≤ 1/3 of body

surface.

Group B - (Moderate – grade2). Infested, with gross lesion affecting > 1/3 but ≤

2/3 of body surface.

Group C - (Severe-grade3). Infested, with gross lesion affecting more than 2/3

of body surface

Group D - Healthy goats for in-contact exposure.

Group E -Healthy (no skin lesion) control.

3.4 PARASITOLOGICAL EXAMINATION

Skin scrapings from infested WAD goats were examined for mites as previously described by

Soulsby, (1998)

3.4.1 Methodology.

A dull scapel blade was held perpendicular to the area of affected skin and used with

moderate pressure to scrape the edges of lesions into a petri dish. The scraped samples were

then transferred into a test-tube, and 10% KOH was added. Samples were mildly heated for

5-6 minutes until it dissolved. It was then centrifuged at 10,000g for 5 minutes. Obtained

23

precipitates were examined under a light microscope at low and high power for presence of

mites or its eggs. Positive cases were classified as clinical sarcoptic mange based on the

presence of mites with long non-jointed pedicels

3.5 SOURCE OF MITE FOR IN-CONTACT TRANSMISSION EXPERIMENT.

Two female goats with severe sarcoptic mange were purchased from an infested farm.

The goats were used to infest healthy goats of group D by housing them together in the same

pen at the animal house as described by Elbers et al., (2000) and Tarigan, (2002).

3.6 CLINICAL MONITORING OF EXPERIMENTAL ANIMALS.

The naturally infested animals were monitored once every week for the progression of

the disease. The in-contact animals in group D were monitored once every week for clinical

manifestations such as pruritus after which they were individually restrained and examined

closely for presence of skin lesions such as erythema, papules, crusts, and alopecia. Skin

scrapings were collected weekly for parasitological examination in each case.

3.7 SAMPLE COLLECTION.

Blood sample (5ml) was collected from each of the goats in groups A to E at the

beginning of the experiment (week 0) and every two weeks, via jugular venipuncture using

sterile needles and syringes. In each case, 2ml of the blood sample was transferred into tubes

containing EDTA for hematological analysis while the remaining 3ml was transferred into

plane test tubes and allowed to clot. Supernatant sera were centrifuged at 10,000g for 10

minutes. Clean sera were extracted, stored at -200C for about 24hrs before they were used for

biochemical and hormonal assay.

The animals were sacrificed humanely at the end of the experiment. The testes and

epididymides were dissected out for epididymal and testicular sperm reserve counts while

skin sections were collected from affected areas of the skin for histopathological studies.

24

3.8 HAEMATOLOGICAL STUDIES

3.8.1 Packed cell Volume( PCV): The microhaematocrit tubes were filled with blood

samples up to three quarter level, via capillary action. One end of the tube was sealed with

plasticein and the tube with its blood content placed in the microhaematocrit centrifuge and

centrifuged at 10,000g for 5 minutes. The PCV was read off as a percentage using the

Microhaematocrit reader (Coles, 1986).

3.8.2 Haemoglobin concentration (Hb): Drabkin’s reagent (ICSH, 1965) assay for Hb

concentration.

Blood sample (0.22ml) was added to 5 ml of Drabkin’s reagent held in a test tube,

and mixed properly. After 5 minutes, the mixture of blood sample and the Drabkin’s solution

was poured into a cuvette, paired with another cuvette, containing only the Drabkin’s reagent.

The absorbance of the diluted blood sample was measured in a spectrophotometer at a

wavelength of 540nm. The haemoglobin concentration in grams per litre was then derived

from the absorbance value by matching against pre-determined reference standards and

calibration curves.

3.8.3 Erythrocyte counts (EC): This was determined using the haemocytometer method

(Coles, 1986). Here, 0.02 ml of blood sample drawn with a micropipette was added to 4 ml

of erythrocyte diluting fluid held in a test tube. A drop of the diluted blood sample was used

to charge the Neubauer chamber before counting the erythrocytes under the microscope at x

40 objective using the tally counter. Erythrocytes in the five small squares of the middle

square of the Neubauer chamber were counted. A factor of 10,000 was used to multiply the

number of cells counted in the five small squares, to get the absolute number of erythrocytes

per microlitre of blood.

25

3.8.4 Erythrocytic indices (erythron values):

These indices were calculated based on the earlier laboratory assay results of PCV,

Hb concentration, and EC (Coles, 1986).

i. Mean corpuscular volume (MCV): This was determined by dividing the PCV by the

EC value determined as described above and then multiplied by a constant of 10.

Values obtained were expressed in femtolitre.

MCV = PCV (%) 10 (in femtolitre)

EC 1

ii. Mean corpuscular haemoglobin (MCH): This was calculated by dividing the

haemoglobin concentration by the EC, already determined, and then multiplied by a

factor of 10. The values were expressed in pictogram.

Hb (gm/dl) x 10

MCH = EC 1 (in picogram)

iii. Mean corpuscular haemoglobin concentration (MCHC): This was calculated by

dividing the haemoglobin concentration by the PCV value already obtained, and the

multiplied by 100. The values were expressed in grams per litre.

Hb (g/dl) x 10

MCH = PCV (%) 1 (in gram per litre)

3.8.5 Total Leucocyte Count (TLC):

This was determined using the haemocytometer method (Coles, 1986). Here, 0.02 ml

of the blood sample collected with a micropipette was mixed with 0.38 ml of white blood cell

diluting fluid held in a test tube. A drop of the diluted blood sample was used to charge the

Neubauer chamber, placed on the microscope stage. White blood cells (leucocytes) were

counted in the four corner squares of the Neubauer chamber under x 40 objective using the

tally counter. The number of leucocytes counted in the four corner squares was multipled by

a factor of 50, to get the total number of leucocytes per microlitre of blood.

26

3.8.6 Differential Leucocyte Counts (DLC):

This was carried out using the stained blood film (Coles, 1986). With the aid of a

micropipette, a drop of the blood sample was placed on a clean microscope slide. The end of

a second slide (spreader) was placed against the surface of the first slide at a 30o angle, and

drawn back into the drop of blood. This action made the drop of blood to spread along most

of the width of the spreader slide (2nd slide). The spreader slide was then pushed forward,

with a steady even rapid motion to make a thin blood smear (film). The prepared smear was

air dried and subsequently stained with May Grounwald-Giemsa stain (Strumia, 1963). The

stained slides were observed under the microscope using the oil immersion objective (x

1000). The differential leucocyte counter was used to count a total of a hundred different

leucocyte cells. Each cell type was recorded as a percentage of the total. The different

percentages of the cells were converted to absolute number of cells per microlitre of blood

using the formula below:

Percentage number of cell type x TLC

100 1

27

3.9 DETERMINATION OF TOTAL SERUM PROTEIN

The determination of Total Serum Protein was carried out using the direct biuret

method as described by Lubran, (1978) for the in vitro determination of total protein in serum

or plasma.

3.9.1 Procedure:

Five clean test tubes were arranged and labeled according to sample identifications.

Also labeled were two test tubes for standards (SD) and two test tubes for blanks (BL)

i.e. SD1, SD2, BL1, and BL2. Added to each sample labeled test tube was 0.02 ml (20

microlitres) of each serum sample.Also added to the test tube labeled standard was

0.02 ml of the standard (SD1 and SD2). Nothing was added to the two blank test

tubes. Thereafter, 1.0ml of Biuret reagent was added to the two blank test tubes.

The content of each test tube was properly mixed and allowed to stand for 10 minutes

at room temperature (20- 25oC).The absorbance of samples and standards were read

off against the blank in a spectrophotometer at 540 nm wavelength.

Total protein concentration for each sample was calculated thus:

Absorance of sample x 5 (g/dl)

Absorbance of standard 1

28

3.10 DETERMINATION OF SERUM ALBUMIN

This was carried out using the Bromocresol green method as described by Dourmas et al.,

1971.

3.10.1 Procedure:

1n each test tube, 0.01ml of serum samples were added for the groups

respectively, while nothing was added to the two blank test tubes. Thereafter,3ml of

the Bromocresol green reagent was added to all the test samples, the standard and

blank tube.The content of each test tube was properly mixed and allowed to incubate

for 5 minutes at 25oC.The absorbance of the test samples and of the standard were

measured against the reagent blank in a spectrophotometer at 540nm wavelength The

albumin concentration for each sample was calculated thus:

Absorbance of sample x Concentration

Absorbance of standard of standard

3.11 DETERMINATION OF SERUM CREATININE

Determination of serum creatinine was based on the modified Jaffe method (Blass et

al, 1974) for the in vitro determination of creatinine in serum, plasma or urine, using the

Quimica Clinica Applicada (QCA) Creatinine test kit (QCA, Spain).

3.11.1 Procedure:

Into each 0.1 ml of serum sample held in a test tube, 1.0 ml of the working reagent

(equal volumes of reagents A and B i.e. 0.5ml of reagent A and 0.5 ml of reagent B) was

added. A stop watch was started before reading off the absorbance of the test sample at the

20th

and 80th

second against a working blank in a spectrophotometer at 546 nm wavelengths.

In the same manner, 0.1 ml of the standard (Reagent C) held in a test tube was mixed with 1.0

ml of the working reagent. The mixture of the standard (Reagent C) and the working reagent

was later transferred into a cuvette.

29

With the aid of a stop watch, the absorbance of the standard was read at the 20th

and

80th

second against a working reagent blank in a spectrophotometer al 546 nm wavelength.

Serum creatinine concentration of each sample was calculated using the formula below:

Change in absorbance (80th

– 20th

) of sample x 2

Change in absorbance (80th

– 20th

second) of sample 1

3.12 DETERMINATION OF SERUM VITAMIN A

Here we employed the colormetric method using Trifluoroacetic acid (TFA) as

described by Neeld and Pearson, (1963).

3.12.1 Procedure:

Duplicate 2 ml aliquots of serum or plasma were pipetted into glass suppressed test

tubes. An equal volume (2 ml) of ethanol is added dropwise with mixing to give a 50%

solution (v/v). At this concentration the protein-retinol bond was disrupted, the protein

precipitated and free retinol and retinyl esters were available for extraction by addition of 3

ml hexane (or pretroleum ether). The tube was stoppered and the contents mixed vigorously

on the vortex mixer for 2 minutes to ensure complete extraction of carotene and vitamin A;

then centrifuged for 5 – 10 minutes at 1000g to obtain a clean separation of phases. Two

mililitres of the upper hexane (or petroleum ether) extract was pipetted into cuvettes and the

cuvettes were capped. Absorbance due to carotenoids at 450 nm is read against a hexane (or

petroleum ether) blank (A450).

After determining A450 the cuvettes were removed and the hexane (or petroleum

ether) was evaporated just to dryness under a gentle stream of nitrogen in a 40 – 60oC water

bath while avoiding splashing on the test tube wall. Just at the point of dryness, the residue

was immediately redissolved and dehydrated by addition of 0.1ml of a mixture chloroform-

acetic anhydride (1:1 v/v).The cuvette containing the sample was placed in the

30

spectrophotometer and 1.0 ml TFA chromagen reagent was added to the cuvette from a rapid

delivery pipette. The absorbance reading (A450) at exactly 15 seconds (t15) and at 30 seconds

(t30) after addition of the reagent were recorded.

3.13 DETERMINATION OF SERUM ZINC AND COPPER.

This is done using Atomic Absorption Spectroscopy as described by Annio, (1964)

and Fernandez and Kahn, (1971).

3.13.1 Procedure:

The blood sample was thoroughly mixed by shaking. The sample was then aspirated

into the oxidizing air-acetylene flame or nitrous oxide acetylene flame. When the aqueous

sample was aspirated, the sensitivity for 1% absorption was observed.

3.14 ADRENAL AND GONADAL STEROID CONCENTRATIONS

3.14.1 Serum Testosterone Determination.

These were determined using ELISA techniques as described by Tiez (1995)

3.14.1A Procedure.

Before proceeding with the assay, all reagents, serum references and controls were

brought to room temperature .The microplate wells for each serum reference, control and test

specimens were formatted to be assayed in duplicate. About 0.010 ml (10µl) of the

appropriate serum reference, control or test specimen were assigned into the respective wells

after which 0.050 ml (50µl) of the working Testosterone Enzyme Reagent was added to all

the wells .The microplate was swirled gently for 20-30 seconds to mix.0.050 ml (50µl) of

Testosterone Biotin Reagent was added to all wells. The microplate was swirled gently for

20-30 seconds to mix and then covered followed by incubation for 60 minutes at room

31

temperature. The contents of the microplate was discarded by decantation and blotted dry

with absorbent paper after which 350µl of wash buffer was added and decanted. This was

repeated for two (2) additional times for a total of three (3) washes followed by addition of

0.100 ml (100µl) of working substrate solution to all wells without shaking. This was

incubated at room temperature for 15 minutes while 0.050ml (50µl) of stop solution was then

added to each well and gently mixed for 15 – 20 seconds. The absorbance in each well was

read at 450nm (using a reference wavelength of 630nm to minimize well imperfections)

using a microplate reader. The results were read within thirty (30) minutes of adding the stop

solution.

3.14.2 Serum Cortisol Determination

This was done as described by Foster and Dunn, (1974)

3.14.2A Procedure

Before proceeding with the assay, all reagents, serum references and controls were

brought to room temperature (20 – 270C). The microplates’ wells were formatted for each

serum reference, control and patient specimen to be assayed in duplicate. 0.025 ml (25µL)

of the appropriate serum reference, control or specimen was poured into the assigned well.

0.050 ml (50µ) of the working Cortisol Enzyme Reagent was added to all wells.The

microplate was swirled gently for 20-30 seconds to mix. 0.050 ml (50µl) of Cortisol Biotin

Reagent was added to all wells. The microplate was swirled gently for 20-30 seconds to mix.

These were covered and incubated for 60 minutes at room temperature. The contents of

the microplate were discarded by decantation and blotted dry with absorbent paper. 350µl of

wash buffer was added decanted. This was repeated for two (2) additional times for a total of

three (3) washes. 0.100 ml (100µl) of working substrate solution was added to all wells

32

without shaking. It was then incubated room temperature for 15 minutes. 0.050ml (50µl) of

stop solution was added to each well and gently mixed for 15 – 20 seconds. The absorbance

in each well at 450nm (using a reference wavelength of 620-630nm to minimize well

imperfections) was read using a microplate reader. The results were read within thirty (30)

minutes of adding the stop solution.

3.15 GONADAL AND EXTRA-GONADAL SPERM RESERVES

The epididymides and the testes were used to assess the sperm reserves of these

organs using the standard haemocytometric method (Amman and Almquist, 1961; Oishi,

2002).

3.15.2 Procedure:

3.15.2A Epididymal Sperm Reserve (ESR):

The epididymides (right and left sides), were dissected out of the testes (right and left

sides), and divided into caput (head), corpus (body), and cauda (tail) segments. Each segment

was transferred into individual clean test tubes, where the epididymal segments (caput,

corpus, and cauda) were minced with ophthalmologic scissors and homogenized for 1 minute

using mortar and pestle, in 20 ml of phosphate buffered saline (Amman and Almquist, 1961;

Oishi, 2002). The homogenate was later filtered using a nylon mesh sieve and 20 µl aliquots

of the filtered homogenate fluid were used in charging the Neubauer chamber for the

appropriate counting of the number of sperms/mg of tissue sample.

3.15.2B Testicular Sperm Reserve (TSR):

With the aid of scalpel blade, a section of each testis was cut off and transferred into a

clean test tube, minced with ophthalmologic scissors and homogenized for 1 minute using

33

mortar and pestle in 10 ml of phosphate buffered saline (Amman and Almquist, 1961; Oishi,

2002). The homogenate was later filtered through a nylon mesh, and 20 µl aliquots of the

filtered homogenate fluid were used in charging the Neubauer haemocytometer for the

appropriate counting of the number of sperms/mg of testis).

3.16 HISTOPATHOLOGY.

This was carried out as described by Bancroft and Stevens, (1977).

3.16.1 Procedure:

Skin sections from S. scabiei infested and control groups of WAD goats were fixed in

10% formol saline and dehydrated in ascending grades of ethanol. Thereafter, the tissues

were cleared in chloroform overnight, infiltrated and embedded in molten paraffin wax. The

blocks were later trimmed and sectioned at 5 – 6 microns. The sections were deparaffinized

in xylene, taken to water and subsequently stained with Haematoxylin and Eosin (H and E)

for light microscopy.

3.17 DATA ANALYSIS

Data obtained were subjected to analysis of variance (ANOVA) and variant means

were separated by the least significant difference (LSD) method, using SPSS statistical

package. Significant differences were accepted at p < 0.05 probability level.

34

CHAPTER FOUR

RESULTS

4.1: PARASITOLOGICAL EXAMINATION

Skin scrapings collected from infested goats revealed eggs, nymphs, larvae and oval

shaped adult mites that were identified as Sarcoptes scabiei on the basis of a rounded body

with four pairs of short legs that scarcely project beyond the body margin and long non-

jointed pedicels as shown in Fig. 3 below.

Figure 3: Sarcoptes scabiei mite isolated from the infested goats, identified by its round

shape, short legs and long non-jointed pedicels (10% potassium hydroxide preparation, x400

magnification)

35

Figure 4: Photomicrograph of an unhatched egg of Sarcoptes scabiei from skin scraping

containing larva (arrow) (10% potassium hydroxide preparation, x 400 magnification).

36

4.2: CLINICAL EVALUATION OF EXPERIMENTALLY EXPOSED GOATS

The chronological sequence of the appearance of clinical signs and lesions for the

experimentally exposed goats is as presented in Table 1 below. Only three of the exposed

(group D) goats developed lesions characteristic of sarcoptic mange. While one died in the

course of the experiment, the 5th

had no visible lesions.

None of the exposed goats showed any clinical sign until day 14 at which time two of

the goats showed signs of pruritus. From day 21 till the end of the study, three(3) goats

presented signs of pruritus. Two of the goats showed areas of erythema, papules and crusts

formation at days 21 and 28 while three showed same at days 35 and 42 of the experiment.

Only one of the goats had focal areas of alopecia at day 21, two at day 28 while the three had

alopecia at days 35 and 42. Mites were not detected in any of the skin scrapings from exposed

goats until day 35 when mite was seen in scrapings from one of the goats and then in two of

the pruritic goats at day 42.

Lesion appeared anterio-posteriorly from the face, nose, ears, around the eyes and the

neck as shown in Figs. 5-7.

37

Table1: Chronology of the appearance of clinical manifestations in the experimentally

exposed WAD goats of group D.

Days post

exposure

Pruritus Erythema Papules Crusts Alopecia Mites in

scraping

0 0/5 0/5 0/5 0/5 0/5 0/5

7 0/5 0/5 0/5 0/5 0/5 0/5

14 2/5 0/5 0/5 0/5 0/5 0/5

21 3/4 2/4 2/4 2/4 1/4 0/4

28 3/4 2/4 2/4 2/4 2/4 0/4

35 3/4 ¾ 3/4 3/4 3/4 1/4

42 3/4 ¾ 3/4 3/4 3/4 2/4

38

Figure 5: A picture of experimentally exposed goat showing crusty,alopecic and lichenified

skin lesions around the ears (arrows) at day 42.

39

Figure 6: A picture of experimentally exposed goat showing scabby, crusty and alopecic

lesions around the eyes (arrows) at day 42.

40

Figure 7: A picture of experimentally exposed goat showing similar lesions around both the

ears and eyes (arrows) at day 42.

41

4.3: HAEMATOLOGY

4.3.1: Packed cell volume, PCV (%)

The mean (± SE) PCV (%) for the infested groups A,B,C,D and control group E

WAD goats is as presented in Table 2. At week 0, all the naturally infested groups had PCV

values significantly (p < 0.05) lower than the control but groups A,B and C were not

significantly (p > 0.05) different although B and C were significantly (p < 0.05) lower than

group D. However, at week 2, the PCV values of groups B and C were still significantly (p <

0.05) lower than the other groups.

At week 4, the group B and C goats which were moderately to severely infested with

Sarcoptes scabiei had a significantly (p < 0.05) reduced mean PCV values relative to groups

D and E. At week 6, the mean PCV values of all the infested groups A, B, C and D were

significantly (p < 0.05) lower than the control group E.

4.3.2: Haemoglobin concentration ,Hb (g/dl)

Table 3 shows the mean (± SE) haemoglobin concentration (Hb) for groups A, B, C,

D and control group (E) WAD goats. At week 0 only the mean Hb values of group B was

significantly (p < 0.05) lower than the control (group E). By week 2, the groups B and C Hb

values were significantly (p < 0.05) lower than the control while at week 4, only the mean Hb

values of group B was significantly (p < 0.05) lower than the control group E, but at week 6,

the Hb values of groups A, B and C WAD goats became significantly (p < 0.05) lower than

the control group E.

4.3.3: Erythrocyte count, EC (x 106

µL)

Table 4 shows the mean (mean ± SE) erythrocyte count (EC) of the naturally infested

groups A, B, C, the experimentally exposed group D and the control group E WAD goats.

The mean EC values of groups B and C were significantly (p < 0.05) lower than the control

group E at week 0. At week 2, there was no significant (p > 0.05) difference among the

groups, although, the mean EC of groups A, B and C were lower than groups D and E.

However, by week 4, the results were similar to what obtained at week 0. By week 6, there

42

was a significant (p < 0.05) reduction in the mean EC values of groups B and C compared to

groups D and E.

4.3.4: Erythrocytic indices

4.3.4A: Mean corpuscular volume, MCV (fl)

Table 5 shows the result of the mean corpuscular volume (MCV) for all the groups. There

was no significant difference between the groups throughout the period of study. However,

the mean MCV values of the infested were lower than the control groups.

4.3.4B: Mean corpuscular Haemoglobin, MCH (pg)

The results of the mean corpuscular haemoglobin (MCH) ( ± SE) of the experimental groups

A, B, C, D and the control (E) WAD goats are presented in table 6.There was no significant

(P>0.05) variation in the mean MCH values of the experimental groups and the control WAD

goats at week 0, 2, and 4. At week 6, the mean MCH of infested groups A, C and D were

lower than the control except that of group B which was significantly (p < 0.05) higher than

the control.

4.3.4C: Mean Corpuscular Haemoglobin Concentration, MCHC (mg/dl)

The mean corpuscular haemoglobin concentrations (MCHC) for all the five groups is

as presented in table 7. No significant (p > 0.05) change was observed at weeks 0 and 2. At

week 4, a significant (p < 0.05) increase in MCHC was observed in group C compared to the

other groups. However at week 6, the MCHC of group B goats became higher than the other

groups (p > 0.05).

4.3.5: Total leucocyte counts, TLC (x 103 cells/µl)

The mean (± SE) TLC of the groups are presented in table 8. The mean TLC values of

the WAD goats in groups B and C increased significantly (p < 0.05) relative to groups A, D

and E throughout the period of study.

43

3.3.6: Differential Leucocyte Counts (DLC)

3.3.6A: Absolute Neutrophil count values (x 103/µl)

Table 9 shows the mean ( ± SE) absolute neutrophil count of the groups of WAD

goats. At weeks 0, 2 and 4 the mean neutrophil count of groups B and C were significantly (p

< 0.05) higher than the other groups.

However, at week 6, the mean values for group C was significantly higher than the other

groups.

3.3.6B: Absolute Lymphocyte Count (x 103µl)

Table 10 shows the mean (±SE) absolute lymphocyte count of the experimental

groups A, B, C, D and control (E) WAD goats. The absolute lymphocyte counts of groups B

and C were higher than the rest of the groups throughout the experimental period.

3.3.6C: Absolute Monocyte Count (x 103µl)

The mean (x ± SE) absolute monocyte count of the groups is presented in Table 11.

There was no significant (p > 0.05) difference among the groups at weeks 0, 2 and 4.

However, by week 6, the mean monocyte count of group C WAD goats was significantly

higher (p < 0.05) than the rest of the groups which were not significantly (p > 0.05) different

from others.

3.3.6D: Absolute Eosinophil Count (x 103/µl)

Table 12 shows the mean ( ± SE) absolute eosinophil count of the experimental

groups. At week 0, the mean eosinophil values of group C goats were significantly higher (p

< 0.05) than groups D and E. Although the eosinophil counts of infested groups remained

higher throughout the period of the experiment, it was not significant ( p > 0.05 ).

3.3.6E: Absolute Basophil Count (x 103/µl)

Table 13 shows the mean ( ± SE) absolute basophil count of the five groups of WAD

goats. All through the period of the study, there was no significant (p > 0.05) difference or

variation in the mean absolute basophil count values of the five experimental groups.

44

Table 2: Mean (± SEM) Packed cell volume values of WAD goats naturally infested and

experimentally exposed to Sarcoptes scabiei.

Values on the same row with different super scripts are significantly (p < 0.05) different.

Experimental

Period

(weeks)

Packed cell volume (%)

Group A

(Mildly infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 24.25±1.38bc

22.00±1.08c

21.50±0.65c

26.75±1.70ab

28.25±0.85a

Week 2 25.50±0.87a

21.75±0.63b

20.75±0.48b

26.50±1.55a

28.25±0.85a

Week 4 22.75±1.65bc

21.25±0.85c 20.00±1.22

c 25.00±1.41

ab 28.00±0.41

a

Week 6 23.25±1.11b

22.00±1.08bc

19.25±0.85c

25.00±1.44b

28.50±0.66a

45

Table 3: Mean (± SEM) haemoglobin concentration of WAD goats naturally infested and

experimentally exposed to Sarcoptes scabiei.

Values on the same row with different superscripts are significantly (p < 0.05) different.

Experimental

period

(weeks)

Haemoglobin concentration (g/dl)

Group A

(Mildly

infested)

GroupB

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 9.65±0.53abc

8.15±0.47c

8.60±0.43ac

9.25±0.70ac

10.05±0.36ab

Week 2 9.18±0.38ab

7.75±0.36b

8.10±0.55b

8.95±0.63ab

9.85±0.40a

Week 4 8.35±0.43ab

7.50±0.54b

8.53±0.66ab

8.83±0.61ab

9.88±0.38a

Week 6 7.35±0.50bc

8.15±047bc

6.85±0.25b

8.55±0.67ac

10.03±0.64a

46

Table 4: Mean (± SEM) Erythrocyte count of WAD goats naturally infested and

experimentally exposed to Sarcoptes scabiei.

Values on the same row with different superscripts are significantly (p < 0.05) different

Experimental

period

(weeks)

Erythrocyte count (x 106

µL)

Group A

(Mild

infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 11.60±0.56ab

10.13±0.25b

10.05±0.44b

11.93±0.95ab

12.63±1.03a

Week 2 11.05±1.06 10.18±0.49 9.95±0.46 12.13±0.74 12.08±1.05

Week 4 10.23±0.41ab

10.05±0.28b

9.88±0.46b

11.60±0.80ab

11.90±0.87a

Week 6 10.40±0.35bc

9.48±0.46b

9.13±057b

11.53±0.87ac

12.53±0.77a

47

Table 5: Mean (± SEM) Mean corpuscular volume of WAD goats naturally infested and

experimentally exposed to Sarcoptes scabiei.

Mean corpuscular volume (fl)

Experimental

period

(weeks)

Group A

(Mildly

infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 21.13±1.79 21.70±0.79 21.43±0.35 22.53±0.49 22.68±1.36

Week 2 23.43±1.33 21.48±0.83 20.98±0.91 21.88±0.36 23.88±1.99

Week 4 22.20±1.07 21.25±1.27 20.33±1.48 21.60±0.36 23.93±1.82

Week 6 22.33±0.54 23.23±0.28 21.30±1.45 21.80±0.84 22.90±0.88

No significant difference between the groups (p > 0.05)

48

Table 6: Mean (± SEM) mean corpuscular haemoglobin of WAD goats naturally infested

and experimentally exposed to Sarcoptes scabiei.

Values on the same row with different superscripts are significantly (p < 0.05) different

Mean corpuscular Haemoglobin (Pg)

Experimental

period

Group A

(Mildly

infested)

Group B

(Moderately

infested)

Group C

(Severely

Infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 8.33±0.49 8.05±0.31 8.63±0.66 7.75±0.24 8.05±0.38

Week 2 8.43±0.57 7.65±0.48 8.25±0.84 7.40±0.15 8.28±0.40

Week 4 8.18±0.28 7.50±0.51 8.63±0.50 7.63±0.05 8.38±0.46

Week 6 7.03±0.25a

8.60±0.18b

7.60±0.61ab

7.40±0.24a

8.03±0.38ab

49

Table 7: Mean (± SEM) Mean Corpuscular Haemoglobin Concentration of WAD goats

naturally infested and experimentally exposed to Sarcoptes scabiei.

Mean Corpuscular Haemoglobin Concentration (mg/dl)

Experiment

al period

(weeks)

Group A

(Mildly

infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 40.50±3.77 37.50±0.65 40.25±2.75 34.50±0.65 35.50±0.87

Week 2 36.00±1.68 35.75±0.85 39.25±3.42 33.75±0.75 35.00±1.68

Week 4 37.25±2.56ab

35.25±2.02a

42.75±2.50b

33.00±0.71a

35.25±1.49a

Week 6 31.50±0.87a

37.00±0.41b

36.25±2.90ab

34.00±0.71ab

35.00±1.91ab

Values on the same row with different superscripts are significantly (p < 0.05) different

50

Table 8: Mean (± SEM) total leucocyte counts of WAD goats naturally infested and

experimentally exposed to Sarcoptes scabiei.

Total leucocyte counts (x 103 cells/µl )

Experimental

period

(weeks)

Group A

(Mildly

infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 13.35±1.31a

19.63±1.14b

17.55±0.35b

13.88±0.66a

13.93±0.66a

Week 2 12.43±1.58a

19.30±1.10b

18.28±1.92b

13.55±0.45a

14.05±0.85a

Week 4 14.38±1.09a

20.35±1.04b

18.35±1.10b

14.63±0.72a

13.75±0.75a

Week 6 15.00±0.69ac

19.63±1.14b

19.98±0.40b

17.25±0.40c

13.85±0.99a

Values on the same row with different superscripts are significantly (p < 0.05) different

51

Table 9: Mean (± SEM) Absolute Neutrophil count values of WAD goats naturally infested

and experimentally exposed to Sarcoptes scabiei.

Absolute Neutrophil count (x 103/µl)

Experimental

period

(weeks)

Group A

(Mildly

infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 5.73±0.65a

9.10±0.78b

7.55±0.54b

5.48±0.04a

5.23±0.36a

Week 2 5.24±0.97a

9.09±0.61b

8.59±1.13b 5.71±0.22

a 5.56±0.60

a

Week 4 6.17±0.71a

10.02±0.65b

8.93±0.88b

6.40±0.61a

5.33±0.35a

Week 6 6.47±0.33a

8.65±1.32ab

10.68±1.31bc

7.81±0.31ab

5.42±0.59a

Values on the same row with different superscripts are significantly (p < 0.05) different

52

Table 10: Mean (± SEM) Absolute Lymphocyte count values of WAD goats naturally

infested and experimentally exposed to Sarcoptes scabiei.

Absolute Lymphocyte Count (x 103µl)

Experimental

period

(weeks)

Group A

(Mildly

infested)

Group B

(Moderately

infested)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 6.77±0.62a

9.65±0.70b

9.05±0.67bc

7.51±0.50ac

8.10±0.21abc

Week 2 7.08±0.63a

9.90±0.74b

9.33±0.36bc

7.94±0.57ac

8.30±0.38ab

Week 4 7.73±0.59a

9.95±0.58b

8.48±0.28a

7.80±0.32a

8.00±0.42a

Week 6 7.96±0.48a

9.83±0.22b

8.75±0.65ab

8.58±0.30ab

7.98±0.49a

Values on the same row with different superscripts are significantly (p < 0.05) different

53

Table 11: Mean (± SEM) Absolute Monocyte Count values of WAD goats naturally infested

and experimentally exposed to Sarcoptes scabiei.

Experimental

period

Absolute Monocyte Count (x 103µL)

Group A

(Mildly

infected)

Group B

(Moderately

infected)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 0.20±0.04 0.34±0.09 0.23±0.9 0.28±0.07 0.29±0.07

Week 2 0.23±0.03 0.25±0.10 0.35±0.13 0.20±0.04 0.26±0.09

Week 4 0.14±0.01 0.15±0.05 0.29±0.14 0.25±0.11 0.28±0.07

Week 6 0.20±0.11a 0.35±0.11

a 0.70±0.11

b 0.39±0.10

a 0.27±0.05

a

Values on the same row with different superscripts are significantly (p < 0.05) different

54

Table 12: Mean (± SEM) Absolute Eosinophil Count values of WAD goats naturally infested

and experimentally exposed to Sarcoptes scabiei

Absolute Eosinophil Count (x 103/µl)

Experimental

period

(weeks)

Group A

(Mildly

infected)

Group B

(Moderately

infected)

Group C

(Severely

infested)

Group D

(Experimentally

Exposed)

Group E

(Control)

Week 0 0.31±0.06ab

0.29±0.04ab

0.40±0.11b

0.18±0.04a

0.11±0.07a

Week 2 0.18±0.05 0.29±0.06 0.29±0.08 0.14±0.05 0.14±0.05

Week 4 0.29±0.07 0.30±0.05 0.24±0.06 0.17±0.07 0.14±0.06

Week 6 0.30±0.07 0.29±0.06 0.35±0.16 0.43±0.06 0.19±0.07

Values on the same row with different superscripts are significantly (p < 0.05) different

55

Table 13: Mean (± SEM) Absolute Basophil Count values of WAD goats naturally infested

and experimentally exposed to Sarcoptes scabiei.

Absolute Basophil count (x 103/µl)

Experimental

period

(weeks)

GroupA

(mildly

infested)

GroupB

(moderately

infested)

GroupA

(Severely

infested )

GroupD

(Experimentally

Exposed)

Group E

(Control)

Week 0 0.04±0.04 0.00±0.00 0.05±0.05 0.00±0.00 0.00±0.00

Week 2 0.00±0.00 0.00±0.00 0.00±0.00 0.00±0.00 0.00±0.00

Week 4 0.04±0.04 0.00±0.00 0.00±0.00 0.00±0.00 0.00±0.00

Week 6 0.04±0.04 0.00±0.00 0.00±0.00 0.04±0.04 0.00±0.00

No significant difference between the groups (p > 0.05)

56

4.5: Serum Biochemical Assay

Statistical analysis showed that the mean total protein was lower in the severely infested

group C (p > 0.05) compared to the rest of the groups while the mean total protein of mildly

infested WAD goats of group A was higher than the rest of the groups (p > 0.05). There was

also no significant variation in the mean total protein of the exposed group D (p > 0.05).

There was no significant variation in mean albumin, globulin and creatinine levels

among the groups (p > 0.05). However, the mean albumin level was lower in the moderate

and severely infested group C (p > 0.05). while the level of creatinine was higher in the

severely infested group C (p > 0.05).. See figures 8 and 9.

57

Figure 8: Mean (±SEM) Serum proteins in WAD goats naturally and experimentally infested

with Sarcoptes scabiei.

Group A- Mildly infested

Group B- Moderately infested

Group C- Severely infested

Group D- Experimentally Exposed (week 0-D0, week 2-D2, week 4-D4, week6-D6)

Group E-(Control)

58

Figure 9. Mean (±SEM) Serum Creatinine in WAD goats naturally and experimentally

infested with Sarcoptes scabiei.

Group A- Mildly infested

Group B- Moderately infested

Group C- Severely infested

Group D- Experimentally Exposed (week 0-D0, week 2-D2, week 4-D4, week6-D6)

Group E-(Control)

59

4.5.3: Serum vitamin A, copper and zinc concentrations

Figures 10 and 11, shows the mean serum vitamin A, copper and zinc concentrations. There

was no significant variation in the mean serum vitamin A levels among the groups (p > 0.05)

but the mean value of the severely infested group C WAD goats were lower (p > 0.05) than

the other groups followed by group A and then B. There was a significant (p < 0.05)

reduction in mean serum copper of group C (p < 0.05) WAD goats compared to the rest of

the groups. Although there was no significant (p > 0.05) variation in mean copper values

between A and B they were still lower than that of group D and E. There was no significant

(p > 0.05) variation in mean serum zinc concentration among the groups. However, the mean

values of the naturally infested groups were lower than groups D and E with values in group

C (severely infested) been the lowest (p > 0.05).

2

Figure10. Mean (±SEM) Serum vitamin A levels in WAD goats naturally and

experimentally infested with Sarcoptes scabiei.

Group A- Mildly infested

Group B- Moderately infested

Group C- Severely infested

Group D- Experimentally Exposed (week 0-D0, week 2-D2, week 4-D4, week6-D6)

Group E-(Control)

3

Figure11. Mean (±SEM) Serum Copper and Zinc levels in WAD goats naturally and

experimentally infested with Sarcoptes scabiei.

Group A- Mildly infested

Group B- Moderately infested

Group C- Severely infested

Group D- Experimentally Exposed (week 0-D0, week 2-D2, week 4-D4, week6-D6)

Group E-(Control)

4

4.5.3 Gonadal and Adrenal Steroid Concentrations.

There was no significant variation (p > 0.05) in mean serum testosterone values

among the groups. However, the mean values of the naturally infested groups A, B, and C

were lower (p > 0.05) than the mean values for the groups D and E with mean

testosterone levels of group C having the lowest value. The result shows that there was no

significant (p > 0.05) variation in the mean serum cortisol concentration among the

groups. However, while the mean cortisol values in groups A and B were higher (p >

0.05) than the rest of the groups, the mean levels in group C was lower (p > 0.05). See

figures 12 and 13.

5

Figure 12. Mean (±SEM) Serum testosterone concentration in WAD goats naturally and

experimentally infested with Sarcoptes scabiei.

Group A- Mildly infested

Group B- Moderately infested

Group C- Severely infested

Group D- Experimentally Exposed (week 0-D0, week 2-D2, week 4-D4, week6-D6)

Group E-(Control)

6

Figure 13. Mean (±SEM) Serum cortisol concentration in WAD goats naturally and

experimentally infested with Sarcoptes scabiei.

Group A- Mildly infested

Group B- Moderately infested

Group C- Severely infested

Group D- Experimentally Exposed (week 0-D0, week 2-D2, week 4-D4, week6-D6)

Group E-(Control)

7

4.4: GONADAL AND EXTRAGONADAL SPERM RESERVE.

4.4.1: Caput epididymal sperm reserve (x 108/ml)

Mean (±SEM) caput epididymal sperm reserve of the five groups of WAD goats

are presented in Fig 14 above. The mean caput epididymal sperm reserves of the naturally

infested WAD goats of groups A, B, C and the experimentally infested group D decreased

significantly (p < 0.05) relative to the mean value of the control group E goats, similarly,

the mean value of group C was significantly (p < 0.05) lower than the values of the other

infested groups. Although the mean value of experimentally infested group D WAD goats

was not significantly (p > 0.05) different from that of groups A and B, it was still

significantly (p < 0.05) lower than the mean caput epididymal sperm reserve of control

group E.

4.4.2: Corpus epididymal sperm reserve (x 108/ml)

Mean (±SEM) corpus epididymal sperm reserve of the five groups of WAD goats

are presented in Fig.15 above. The mean corpus epididymal sperm reserves of the

naturally infested WAD goats of groups A, B, C and experimentally infested group D

were significantly (p < 0.05) lower relative to the mean values of control group E goats.

The mean values of group C was significantly (p < 0.05) lower than the other groups.

Although the mean values of in contact group D WAD goats was not significantly (p >

0.05) different from that of groups A and B.

4.4.3: Cauda epididymal sperm reserve (x 108/ml)

Figure16 represents the mean (±SEM) cauda epididymal sperm reserve of the

experimental WAD goats. The observed reduction in the cauda epididymal sperm reserve

values of the goats in groups A, B and C differed significantly (p < 0.05) from the mean

values of in- contact group D and control group E. There were no observed significant

differences in the mean cauda epididymal sperm reserves of goats in the three naturally

infested WAD groups A, B and C, but mean values reduced with increased severity of

lesion. Although the mean value of in-contact group D WAD goats was lower than the

control, it was not statistically significant (p > 0.05).

8

4.4.4: Mean total epididymal sperm reserve (ESR) (x 108/ml)

The mean (±SEM) epididymal sperm reserve is presented in Figure 17. The

naturally infested WAD goats (groups A, B, C) had significantly (p < 0.05) lower mean

epididymal sperm reserve relative to the in-contact group D and control group E.

Although the mean values of the in-contact group D was significantly (p < 0.05) higher

than groups A, B and C, it was significantly (p < 0.05) lower than the control group E.

The mean values of the naturally infested groups B and C decreased significantly (p <

0.05) based on the degree of skin lesion.

4.4.5: Right testicular sperm reserve (x 108/ml)

The mean right testicular sperm reserve decreased significantly (p < 0.05) in

groups A, B and C relative to the control group E. The mean values of the right testicular

sperm reserve in groups A, B and C were not significantly (p > 0.05) different although

there was a decrease that correlates with the degree of skin lesion. There was a higher

mean right testicular sperm reserve in in-contact groups relative to the control although

this was not significant (p > 0.05).See figure 18.

4.4.6: Mean left testicular sperm reserve

There was a significant (p < 0.05) decrease in mean left testicular sperm reserve in

group C WAD goats (severely infested group) compared to groups D and E. Although

the mean values of left testicular sperm reserve in groups A and B were not significantly

different (p > 0.05) they were still lower than the mean values for the groups D and E.

There was no significant (p > 0.05) difference in the mean values of in-contact group D

and the control E. See figure 19.

4.4.7: Mean combined testicular sperm reserve

Figure 20 shows the mean combined testicular sperm reserve. There was no

significant (p > 0.05) difference in values of CTSR among the naturally infested groups

A, B, and C, but they were significantly (p < 0.05) lower than groups D and E. There was

also no significant difference between the in-contact group D and control group E.

9

Experimental groups.

Figure 14: Mean (± SEM) caput epididymal sperm reserve of WAD goats infested with

Sarcoptes scabie and the control E.

Mean (±SEM) caput

epididymal sperm

reserve (x108/ml)

10

Figure 15: Mean (± SEM) corpus epididymal sperm reserve of WAD goats infested with

Sarcoptes scabie and the control E.

Mean (±SEM)

corpus epididymal

sperm reserve

(x108/ml)

11

Figure 16: Mean (± SEM) cauda epididymal sperm reserve of WAD goats infested with

Sarcoptes scabie and the control E.

Mean (±SEM) cauda

epididymal sperm

reserve (x108/ml)

12

Figure 17: Mean (± SEM) total epididymal sperm reserve of WAD goats infested with

Sarcoptes scabie and the control E.

Mean (±SEM) total

epididymal sperm

reserve (x108/ml)

13

Figure 18: Mean (± SEM) right testicular sperm reserve of WAD goats infested with

Sarcoptes scabie and the control E.

Mean (±SEM) right

testicular sperm

reserve (x108/ml)

14

Figure 19: Mean (± SEM) left testicular sperm reserve of WAD goats infested with

Sarcoptes scabie and the control E.

Mean (±SEM) left

testicular sperm

reserve (x108/ml)

15

Figure 20: Mean (± SEM) combined testicular sperm reserve of WAD goats infested

with Sarcoptes scabie and the control E.

.

Mean (±SEM)

combined testicular

sperm reserve

(x108/ml)

62

4.6 HISTOPATHOLOGY.

Sections from control goats showed a normal epidermis overlying a normal

dermis with sebaceous glands and hair follicles (Fig.21). Sections from Sarcoptes scabiei-

infested goats showed non-specific skin lesions such as hyperkeratosis and hyperplastic

epidermis with elongation of the dermal papillae/acanthosis. These changes were more

prominent in moderate and severely infested groups (Figs.23-25).There were

subcorneal/intracorneal epidermal pustules (Figs.22-25) which in most cases were

sloughed off along with the keratinized layer of the epidermis mostly in groups with

moderate and severe infestation. In many animals, there were sections of mites and

severe polymorphonuclear and mononuclear infiltration of the papillary dermis and

epidermis (Figs.22-24). Intense papillary dermal fibrosis was observed in severely

infested goats which led to granulation tissue deposition (Fig.26). Affected hair follicles

were empty (devoid of shaft) and filled with keratin in many of the sections. Summary of

histologic changes in the skin of various groups is as presented in Table 17. Vacuolation

of keratinocytes was more in mild and in-contact groups (Fig.27) while hyperaemia of the

papillary dermis was more prominent in moderate and severely infested groups.

Inflammatory cells infiltration of the papillary dermis was more in the moderate and

severely infested groups and consisted of plasma cells, macrophages, polymorphs,

lymphocyte and mast cells. Section of parasites was more evident in moderate and severe

infestations.

63

Table.17. Summary of histologic lesions in the five groups of experimental animals.

S/No. Experimental Group

Group A

(Mild)

Group B

(Moderate)

Group C

(Severe)

Group D

(In-

contact)

Group E

(Control)

Lesion

1 Parakeratosis ++ ++++ +++ ++ *

2 Hyperkeratosis ++ ++++ +++ ++ *

3 Acanthosis/epidermal

hyperplasia

++ +++ ++++ ++ *

4 Fibroblasia

(Scarring)

+ +++ ++++ + *

5 Hyperaemia + +++ +++ ++ *

6 Vacuolation of

keratinocytes

+++ + + +++ *

7a Plasma cell + ++ +++ ++ *

-b Macrophages + ++ +++ ++ *

-c Polymorphs ++ +++ ++ ++ *

-d Lymptrocytes + ++ +++ ++ *

-e Mast cells + +++ ++ ++ *

8 Pustules + +++ ++ + *

9 Sections of parasite + +++ ++ + *

*Not Noticeable

+ mild

++ moderate

+++ severe

++++ Very severe

64

Figure 21: Photomicrograph of skin section from group E (control) goats showing normal

epidermis (black arrow), the dermis (D) and hair follicles (white arrow). H and E x 100.

.

D

65

Figure.22: Photomicrograph of a skin section from group A (mildly infested) goats

showing hyperkeratosis (H) and epidermal pustules (EP). H and E x 400.

H

EP

66

Figure 23: Photomicrograph of skin section from group B (moderately infested) goats

showing degenerating section of the mite (black arrow), pustule (P), rete peg formation

(white arrow) and mononuclear cellular infiltration of the papillary dermis (PD).H and E

x 100.

PD P

67

Figure 24: Photomicrograph of skin section from group B (moderately infected) goats

showing epidermal pustules (black arrow) and hyperplasia (white arrow).H and E x 400.

68

Figure 25: Photomicrograph of skin section from group C (severely infested) goats

showing a section of the parasite (black arrow), hyperplastic epidermis (H), severe

mononuclear cell infiltration of the dermis (PD) and pustules (white arrow).H and E x

100.

P H

PD

H

PD

H

69

Figure 26: Photomicrograph of skin section from group C (severely infested) goats

showing intense granulation tissue formation (DF). Note the sloughed off epidermal area

(arrow).H and E x 100.

DF

70

Figure 27: Photomicrograph of skin section from group D (in-contact) goats showing

vacuolation of keratinocytes (black arrows) and epidermal parakeratosis (white arrow).H

and E x 400.

E

D

71

CHAPTER FIVE

DISCUSSION AND CONCLUSION

5.1 DISCUSSION

This study has shown that a wide variation exist in the susceptibility of the WAD

goats (group D) to natural Sarcoptes scabiei infestation. Only three out of the five goats

introduced to the two seeder goats showed gross lesions. Although, one of the goats died

due to circumstances that we do not consider to be directly related to scabies, the reason

for non-infestation or lack of clinical disease in the fourth goat is not discernable. Some

factors have been speculated to facilitate transmission of Sarcoptes scabiei in flocks.

They include immunological state of the animals, nutritional status, stocking density,

dominance interaction, frequency of contact and pen size. (Hawkins et al., 1987; Thoday,

1993; Davies, 1995; Wondwossen et al., 2010).There was no indication that the goats

used for this experiment suffered from any immune-deficiency, but we did not assess

immune status before the study. The pen size was moderate but dominance interaction

may be a factor as the five goats were males while the seeder goats were female. This was

intentionally done to increase the frequency of contact.

The gross and histologic lesions distribution on the in-contact goats that

developed clinical disease was similar to those earlier described (Wondwossen et al.,

2010; Nektarios et al., 2011).This work showed that the gross lesions of Sarcoptic mange

in the in-contact goats started from the head region beginning with the nose, face, ears,

eye lashes, and lateral neck in all the three infested goats. Although site predilection of

Sarcoptes scabiei has been described in pigs and humans (Johnson and Mellanby, 1942;

Davies and Moon, 1990), the factors affecting the site predilection in these goats are not

apparent. The distribution of the lesions may be due to the fact that bucks or goats in

general explore their pen mates more using the head. Thus, the lesions were anterio-

72

posterior in distribution (i.e. progressively from the head to the tail region).This study has

established that experimental contact transmission of scabies in WAD goats is possible

as seen in a field situation when one or more infested animal(s) are introduced into

susceptible population. Mites were only demonstrated in two out of the four (50%)

remaining goats by day 42 of the study. It has also shown that in the WAD goats,

demonstration of mites in skin scraping of infested goats is most likely to reveal mites in

moderate to severely infested animals. Cargill and Dobson (1979) were the first to

undertake a contact transmission experiment in pigs where they observed that skin

scrapings were of value only in the chronic form of sarcoptic mange.

The marked reduction in PCV, Hb and EC values seen in the naturally infested

goats of group A, B and C throughout the period of study and in group D by the 6th

week

of the study compared to the control shows that mange is associated with anaemia at later

stages of infestation. Similar results have also been reported in rabbits and dogs with

severe and short term advanced sarcoptic mange (Arlian et al; 1988a, 1995), experimental

sarcoptic mange in camels (Parmar et al., 2005), sheep (Hafeez et al.,2007) and goats

(Ujjwal and Dey, 2010), even though they did not relate such changes in erythrocytic

indices to the severity of mange. However, this result is in contrast to that of Chineme et

al., (1979) who observed no change in the blood of sheep suffering from sarcoptic mange.

It could be that the sheep they studied were under one form of supplementation or the

other during the course of the disease since this was not highlighted in the case report.

The increase in TLC which was accompanied by a significant (p < 0.05) increase in both

the neutrophil and lymphocyte counts in groups B and C compared to groups A and E, is

indicative of a systemic inflammatory status in mange infestation. This could be due to

invasion of bacteria from cutaneous lesions or immunomodulatory activity of mange

products. However, the increased monocyte count in group C at week 6 may be due to

73

increased need for phagocytosis of dead cellular debris in the severely affected animals.

The increase in eosinophil counts of infested groups A, B and C compared to the control

as observed in this study has been reported in sarcoptic mange infested wombats (Skerrat

et al., 1999), red foxes (Little et al., 1998), raccoon dogs (Kido et al., 2011) and dogs

(Arlian et al., 1995). This increase might have been induced by parasites in the skin as

eosinophils are known to be the common cellular response in many parasitic infestations.

It is also an indication of type I hypersensitivity reaction.

The marked reduction in total protein values of the severely infested group C

goats compared to the rest has also been reported (Kido et al., 2011). This was attributed

to loss of appetite and resultant malnutrition usually associated with debilitated sarcoptic

mange infested animals. The observation was further substantiated from necropsy

findings in most of the animals in group C in which there was serous atrophy of the

pericardial and subcutaneous fats. The mean albumin and globulin values decreased with

increasing severity of infestation. The reductions could also be due to loss of plasma

proteins from the exudative dermatitis as has been previously reported (Pence et al.,

1983; Kamboj, 1991; Dadlich and Khanna, 2008).The A/G ratio was not clinically

significant except that of the moderately infested group B which was less than 1 and

might be attributed to malnutrition. The high creatinine concentration observed in the

severely infested group C WAD goats could be due to glomerulonephritis usually

associated with complicated sarcoptic mange infestation (Svartman, et al., 1972; Burgess,

1994; Nakagawa, 2009; Kido et al., 2011) or false elevations resulting from non-

creatinine chromogens such as acetoacetic acid (Ketone body) due to chronic malnutrition

or debilitation. There were reductions in serum vitamin A, zinc and copper concentrations

in all the infested groups compared to the control. Although, there is no report available

to me in the literature on the status of vitamin A, zinc or copper concentrations in

74

Sarcoptes scabiei-infested animals, recent debates have associated sarcoptic mange with

increased free radical generation (Dimri et al., 2008; Camkerten et al., 2009; Ujjwal and

Dey , 2010;) . Carotenoids, zinc and copper are well known nutritional antioxidants in

addition to their other functions in the body (Bickers and Athar, 2006; Dimri et al., 2008).

Observations on the adrenal and gonadal steroid concentrations showed that sarcoptic

mange did not affect cortisol concentration while testosterone concentration decreased

with the severity of mange. The initial perception was that infested animals would be

severely stressed and that such stress could impact on the immune system consequent

upon cortisol release. One can only assume or attribute this fact to the innate ability of the

WAD goats to withstand harsh conditions, as information in the literature is presently not

available to me if any. An interesting part of this work was the reduction in epididymal

and testicular sperm reserves in all the infested groups of WAD goats compared to the

control. Scrotal dermatitis which is sometimes associated with mange could also result in

increased testicular temperature. Testicular degeneration with consequent spermatogenic

arrest has been reported in a ram with scrotal acariasis (Rhodes, 1976) just as Skerrat et

al., (1999) reported that gonads of mature wombats with sarcoptic mange had minimal

activity. The testicular degeneration and associated low sperm reserves indicate that

sarcoptic mange may be able to hinder reproduction. This was also speculated by

Overskaug, (1994) and Little et al., (1998).

The histopathologic changes observed in the skin in this study were non-specific

but the presence of sections of mites and granulation tissues seen in severely infested

goats are noteworthy. These were related to the severity of infestation and thus could

serve as markers for grading the severity of the disease. This has also been reported in

raccoon dogs suffering from sarcoptic mange (Ninomiya and Ogata, 2005).

75

5.2 CONCLUSION.

This study has evaluated the pathophysiology of sarcoptic mange in male West

African Dwarf goats and has indeed established that:

i. Sarcoptic mange can induce abnormal hematological and biochemical changes

based on the severity of disease which is also dependent on duration of infestation.

ii. The disease leads to possible nutritional deficiency (as seen in low total

protein, copper, zinc and vitamin A levels) thus giving a clue on the possible

relevance of nutritional/antioxidant incorporation in management and control

regimens.

iii. Sarcoptic mange can be experimentally transmitted by contact without

modification of skin or nutrition of susceptible goats.

iv. Sarcoptic mange can impair reproductive function in male goats.

v. Skin scraping is of little diagnostic value at the early stage of the disease (i.e.

when less than 30% of the body surface is affected).

In the light of the above, there is need to carry out further studies on the effect of various

treatment regimen and control measures on the observed changes.

76

REFERENCES

Adeloye, A.A. (1985). Water utilization by the goat fed with maize cob. Nutrition Report

International 32(6), 1461-1466.

Adeloye, A.A. (1998). The Nigerian Small Ruminant species. Corporate Office Max.

Ilorin, Nigeria: 7-8.

Alexander, J, O. (1984). Arthropods and human skin. Springer-Verlag, Berlin, Germany.

Amman, R.P. and Almquist, J.O. (1961). Reproductive capacity dairy bulls. 1. Technique

for direct measurement of gonadal and extragonadal sperm reserves.Journal of

Dairy Science. 44:1537-1539.

Amsalu, D., Bewket, S., Kassa, T., Tefera, T., Gezahgne, M., Dagne, M. and Shihun, S.

(2000). Mange: A disease of growing threat for the production of small ruminants

in Amhara National Regional State. Proceedings of conference on the

opportunities and challenges of enhancing goat production in East Africa,

Awassa, Ethiopia, November 10-12: 80-91.

Anderson, R.K. (1981). Norwegian scabies in a dog: A case report. Journal of the

American Animal Hospital Association, 17: 101-104.

Anderson, D.E.,Rings, D. M. and Pugh,D. G. (2002).Diseases of the integumentary

system:In Sheep and Goat Medicine. D.G.Pugh,Ed.,pp 97-422, WB Saunders,

Philadelphia, Pa, USA.

Andrews, J.R.H. (1983). The origin and evolution of host association of Sarcoptes scabiei

and the subfamily Sarcoptinae Murray. Acarologia, 24:85-94.

Annio, J.S. (1964). Clinical Chemistry: Principles and Procedures. 3rd

Edition. Little,

Brown and Company, Boston.

Argenziano, G., Fabbrocini, G. and Delfino. M. (1997). Epiluminescence microscopy.

Archives of Dermatology, 133:751-753.

Arlian, L.G. (1989). Biology, host relations and epidemiology of Sarcoptes scabiei.

Annual Reviews of Entomology, 34: 139-161.

Arlian, L.G., Runyan, R.A. and Este, S.A. (1984a). Cross infectivity of Sarcoptes scabiei.

Journal of the American Academy for Dermatology, 10:979-986.

Arlian, L.G., Runyan, R.A., Achar, S. and Estes,S.A. (1984b). Survival and infectivity of

Sarcoptes scabiei var. canis and var. hominis. Journal of the American Academy

for Dermatology, 11:210-215.

77

Arlian, L.G., Ahmed, M. and Vyszenki-Moher, D.L. (1988a). Effects of Sarcoptes scabiei

var canis (Acari: Sarcoptidae) on blood indexes of parasitized rabbits. Journal of

Medical Entomology, 25: 360-369.

Arlian, L.G., Ahmed, M., Vyszenski-Moher, D.L., Estes, S.A. and S. Achar. (1988b).

Energetic relationships of Sarcoptes scabiei var. canis (Acari: Sarcoptidae) with

the laboratory rabbit. Journal of Medical Entomology, 25:57-63.

Arlian, L.G., Bruner, R.H., Stuhlaman, R.A., Ahmed, M., Vyszenski-Moher, D.L. and

Moher, D.L.V. (1990). Histology in hosts parasitized by Sarcoptes scabiei. The

Journal of Parasitology, 81: 889-894.

Arlian, L.G., Morgan, M.S., Vyszenski-Moher, D.L. and Stemmer, B.L. (1994a).

Sarcoptes scabiei: The circulating antibody response and induced immunity to

scabies. Experimental Parasitology, 78: 37-50

Arlian, L.G., Rapp, C.M., Vyszenski-Moher, D.L. and Morgan M.S. (1994b).Sarcoptes

scabiei: Histopathological changes associated with acquisition and expression of

host immunity to scabies. Experimental Parasitology, 78:51-63.

Arlian, L.G., Rapp, C.M. and Morgan M.S. (1995). Resistance and immune response in

scabies-infested hosts immunized with Dermatophagoides mites. American

Journal of Tropical Medicine and Hygiene, 52: 539-545.

Arlian, L.G., Morgan, M.S., Rapp, C.M. and Vyszenski-Moher, D.L. (1996).The

development of protective immunity in canine scabies. Veterinary Parasitology,

62:133-142.

Arlian, L.G., Morgan, M.S., Estes, S.A., Walton, S.F., Kemp, D. J. and Currie, B. J.

(2004). Circulating IgE in patients with ordinary and crusted scabies. Journal of

Medical Entomology, 41:74-77.

Arlian, L.G., Morgan, M.S. and Paul,C.C. (2006). Evidence that scabies mites

(Acari:Sarcoptidae) influence production of interleukin-10 and the function of T-

regulatory cells (Trl) in humans. Journal of Medical Entomology, 43:283-287.

Bals, A. and Rath, S. S. (2006). Studies on hematobiochemical alterations due to

sarcoptic mange in buffalo calves. Indian Veterinary Journal, 83: 230-231.

Bancroft, J.D. and Stevens, A. (1977). Theory and Practice of Histological Techniques.

Churchill Livingstone, Edinburgh. 16-64.

Beck, A. L. (Jr). (1965). Animal scabies affecting man. Archives of Dermatology, 91:54-

55.

Bezold, G., Lange, M., Schiener, R., Palmedo, G., Sander, C.A., Kerscher, M. and Peter,

R.U. (2001). Hidden scabies: Diagnosis by polymerase chain reaction. British

Journal of Dermatology, 144:614-618.

78

Bickers, D.R. and Athar ,M. (2006). Oxidative stress in the pathogenesis of skin disease.

Journal of Investigative Dermatology, 126, 2565-2575.

Blass, K.G., Thiebert, R.J. and Lam, L.K. (1974). A study of the mechanism of the Jaffe

reaction. Journal of Clinical Chemistry and Clinical Biochemistry, 12:336-343.

Bornstein, S. and Zakrisson, G. (1993). Humoral and antibody response to experimental

Sarcoptes scabiei var vulpes infection in the dog. Veterinary Dermatology, 4: 107

– 110.

Bornstein, S. and Wallgren, P. (1997). Serodiagnosis of sarcoptic mange in pigs.

Veterinary Record, 141:8-12.

Bornstein,S., Zarkrisson, G. and Thebo, P. (1995). Clinical picture and antibody response

to experimental Sarcoptes scabie var sius infection in red foxes (vulpes vulpes).

Acta Veterinaria Scandinavia, 36, 509-519.

Bornstein, S., Thebo, P. and Zakrisson,G. (1996). Evaluation of an enzyme linked

immunosorbent assay (ELISA) for the serological diagnosis of canine sarcoptic

mange. Veterinary Dermatology, 7:21-27.

Bornstein, S.T., Morner, T. and Samuel, W.M. (2001). Sacroptes scabiei and Sarcoptic

mange: In Parasitic diseases of Wild Mammals, W.M. Samuel, M.J. Pybus, and

A.A. Kocan, Eds., Iowa state University press, Ames lowa, USA, 2nd

Edition.

107-119.

Brook, I. (1995). Microbiology of secondary bacterial infection in scabies lesions.

Journal of Clinical Microbiology, 33:2139-2140.

Burgess, I. (1994). Sarcoptes scabiei and scabies. Advances in Parasitology, 33:235-292.

Cabrera, R., Agar, A. and Diehl, M.V. (1993). The immunology of scabies. Seminars in

Dermatology, 12: 15-21.

Camkerten, I., Sahin, T., Borazan, G., Gokcen, A., Erel, O. and Das, A. (2009).

Evaluation of blood oxidant/antioxidant balance in dogs with sarcoptic mange.

Veterinary Parasitology, 161 (1-2):106 - 109.

Chevrant-Breton, J., Desrues, E., Auvray, E., Guiguen, C. and DeCertaines, J. (1981). IgE

seriques et gale humaine. Annals of Dermatology and Venereology, 108: 979-

983.

Chineme, C.N., Bida, S.A. and Nauru, S. (1979). Sarcoptic mange of sheep in Kaduna

State, Nigeria. Bulletin of Animal Health & Production. 27:41-45.

Chosidow, O. (2006). Scabies. New England Journal of Medicine, 354:1718-1727.

Coles, E.H. (1986). Veterinary Clinical Pathology, 4th

Edition W.B. Saunders Company,

Philadelphia, USA.

79

Currie, B.J., Harumal, P., McKinnon, M. and Walton,S.F.(2004). First documentation of

in- vivo and in-vitro ivermectin resistance in Sarcoptcs scabiei. Clinical Infectious

Diseases. 39:8-l2.

Cargill, C. E. and Dobson K. J. (1979). Experimental Sarcoptes scabiei Infestation in

pigs: II. Effects on production .Veterinary Record, 104: 3306.

Curtis, C F. (2004). Current trends in the treatment of Sarcoptes, Cheyletiella and

Otodectes mite infestations in dogs and cats. Veterinary Dermatology, 15(2):108-

114.

Dalapati, M.R., Bhowmik, M.K. and Sarkar, S. (1996). Clinico-hematological,

biochemical and pathomorphological changes of scabies in goats. Indian Journal

of Animal Science, 66:351-354.

Darzi, M.M., Mir, M.S., Shahardar, R.A. and Pandit, B.A. (2007). Clinico-pathological,

histochemical and therapeutic studies on concurrent sarcoptic and notoedric

acariosis in rabbits (Oryctolagus cunniculus). Veterinaski Arkhiv, 77(2): 167-175.

Davies, P. R. (1995). Sarcoptic mange and production performance of swine: a review of

the literature and studies of associations between mite infestation, growth rate and

measures of mange severity in growing pigs. Veterinary Parasitology, 60: 249-64.

Davies, D. P, and Moon R. D. (1990). Density of itch mite Sarcoptes scabiei on

experimentally infested pigs. Journal of Medical Entomology, 27; 391-8.

Dadlich,H. and Khanna, R. (2008).Pathological, hemato-biochemical and immunological

studies of cutaneous ectoparasitosis in dogs. Proceedings, The 15th

Congress of

FAVA-OIE Joint Symposium on Emerging Diseases.

Devendra, C. (1976). Productivity of goats and sheep in Malaysia 1. The potential

contribution from goats. Bulletin. Ministry of Agriculture, Kuala Lumpur,

Malaysia. 144, 29-47.

Devendra, C. and Burns, M. (1983). Goat production in the tropics. Commonwealth

Agricultural Bureaux Carlton House Terrace, London SW. 1:90-91.

Dimri,U.R., Ranjan, N., Kumar, M. C., Sharma, D., Swarup, B. and Kataria, M.

(2008).Changes in oxidative stress indices, zinc and copper concentration in

canine demodicosis. Veterinary Parasitology, 154:98-102.

Dorny, P., Van Wyngaarden, T.,Vercruysse, J., Symoens, C. and Jalila, A. (1994). Survey

on the importance of mange in the aetiology of skin lesions in goats in Peninsular

Malaysia. Tropical Animal Health and Production, 26(2): 81-86.

Doumas, B.T., Watson, W.A and Biggs, H.G. (1971). Albumin standards and the

measurement of serum albumin with Bromocresol Green. Clinical

Chemistry, 31: 87.

80

Elbers,A.R., Rambags,G., Van Der Heijden,H. M. and Hunneman, W. A. (2000).

Production performance and pruritic behaviour of pigs naturally infected by

Sarcoptes scabiei var suis in a contact transmission experiment. Veterinary

Quarterly, 22:145-149.

Falk, E.S. (1980). Serum immunoglobulin values in patients with scabies. British Journal

of Dermatology, 102: 57-61.

Falk,E.S. (1981). Serum IgE before and after treatment for scabies. Allergy, 36: 167-174.

Falk, E.S. and Bolle, R. (1980a). IgE antibodies to house dust mite in patients with

scabies. British Journal of Dermatology, 102: 283-288.

Falk,E.S. and Bolle,R. (1980b). In-vitro demonstration of specific immunological

hypersensitivity to scabies mite. British Journal of Dermatology, 103: 367-373.

Falk,E.S. and Eide, T.J. (1981).Histologic and clinical findings in human scabies.

International Journal of Dermatology, 20:600-605.

Falk, E.S. and Matre, R., (1982). In situ characterization of cell infiltrates in the dermis of

human scabies. American Journal of Dermatopathology, 4: 9-15.

Fernandez, F.J. and Kahn,H.L. (1971).Clinical methods for atomic absorption

spectroscopy. Clinical Chemistry Newletter, 3:34.

Fernandez, N., Torres, A. and Ackcrman,B. (1977).Pathologic findings in human scabies.

Archives of Dermatology, 113:320-324.

Fischer,K.,Holt,D.G., Harumal,P., Currie,B.J., Walton,S.F. and Kemp.D.J.(2003).

Generation and characterization of cDNA clones from Sarcoptes scabie var

hominis for an expressed sequence tag library: identification of homologues of

house dust mite allergens. American Journal of Tropical Medicine and Hygiene,

68:61-64.

Folz, S.D. (1984).Canine scabies : Sarcoptes scabiei infection. The Compendium on

Continuing education from the Practicing Veterinarian, 176: 176-184.

Foster, L. and Dunn, R. (1974).Single antibody technique for radioimmunoassay of

cortisol in unextracted serum or plasma. Clinical Chemistry, 20:365.

Francis,P.A. (1988).Some aspects of sheep and goat management in southeast, Nigeria.

ILCA bulletin, 40: 20-25.

Giadinis,N.D., Farmaki,R., Papaioannou,N., Papadopoulos,E., Karatzias, H. and

Koutinas, A.F.(2011).Moxidectin efficacy in a goat herd with chronic and

generalized sarcoptic mange. Veterinary Medicine International, 10:1-4.

Gorakh,M., SuchitraSen,D., Kumar,R. and Sahani,M.S.(2000).A study of clinical,

hematobiochemical and histopathological aspect of mange in camels. Journal of

Veterinary Parasitology, 14(1): 29-30.

81

Gross,T.L., Ihhrke, P.J. and Walder, E.J. (1992).Diseases of the dermis. In: R.W.

Reinhardt, Editor, Veterinary Dermatopathology: A Macroscopic and Microscopic

Evaluation of Canine and Feline Skin Diseases, Mosby-Yearbook, St. Louis: 123-

125.

Haas,N. and Sterry,W. (2001).The use of Epiluminescence light microscopy to monitor

the success of antiscabietic treatment. Archives of Dermatology, 37:1656-1657.

Hafeez,U.A., Zia-Ud-Din,S., Zafar,I., Abdul, J. and Zahida, T. (2007).Prevalence of

sheep mange in District Dera Ghazi Khan (Pakistan) and Associated

hematological/biochemical disturbances. International Journal of Agriculture and

Biology, 9(6):917-920.

Hancock, B.W. and Milford-ward, A. (1974). Serum immunoglobulins in scabies.

Journal of Investigative Dermatology, 63:482-484.

Harumal, P., Morgan, M.S., Walton, S.F., Holt, D.C., Rode, J., Arlian,L.G., Currie, B.J.

and Kemp,D. J. (2003). Identification of a homologue of a house dust mite

allergen in a cDNA library from Sarcoptes scabiei var hominis and evaluation of

its vaccine potential in a rabbit/s.scabiei var.canis model. American Journal of

Tropical Medicine and Hygiene, 68:54-60.

Hawkins, J. A., McDonald, R. K. and Woody, B. J. ( 1987). Sarcoptes scabiei infestation

in a cat. Journal of American Veterinary Medical Association, 190:1572-1573.

Heilesen, B. (1946). Studies on Acarus scabiei and scabies. Acta Dermatologia and

Venereologia, 26(Suppl.):365-370.

Hejazi, N, and Mehregan, A.H. (1975). Scabies: histological study of inflammatory

lesions. Archives of Dermatology, 111: 37-39.

Hoefling, K.K. and Schroeter,A.L. (1980).Dermatoimmunopathology of scabies. Journal

of the American Academy Dermatology, 3:237-240.

Hollanders, W. J., Vercruysse, S. R. and Bornstein,S.(1997).Evaluation of an enzyme-

linked immunosorbent assay (ELISA) for the serological diagnosis of sarcoptic

mange in swine. Veterinary Parasitology, 69:117-123.

Ibrahim, K.E. and Abu-samra, M.T. (1987).Experimental transmission of a goat strain of

sarcoptes scabiei to desert sheep and its treatment with ivermectin. Veterinary

Parasitology, 26(1-2): 157-164.

ICSH, (1965). International Council for Standardization in Hematology (ICSH). In

Guidelines on Standard Operating Procedures for Hematology.

Haemoglobinometry.WHO.www.searo.who.int/en.

ILCA (1987). Annual Report of the International Livestock Centre for Africa. Addis

Ababa, Ethiopia.

82

ILRI, (1999).Making the livestock revolution work for the poor, Annual Report,

International Livestock Research Institute, Nairobi, Kenya. 1-32.

Jackson, P.G.G., Richards, H.W. and Lloyd, S. (1983). Sarcoptic mange in goats.

Veterinary Record, 112(14):330.

Jajasuriya, M.C.N. (1999). Summary of the coordinated project on development of feed

supplementation strategies for improving the productivity of dairy cattle on small

holder farmers in Africa. Annual Production Health Section, IAEA. 1-5.

Johnson,C. G. and Mellanby, K. (1942).The parasitology of human scabies. Parasitology,

34: 285-290.

Kambarage, D.M. (1992). Sarcoptic mange infection in goats. Bulletin of Animal

Production in Africa, 40: 239-244.

Kamboj, D. S. (1991).Clinical studies on bacterial and parasitic dermatitis with special

reference to diagnosis and treatment. M.V.Sc thesis, Punjab Agricultural

University,Ludhiana.

Karin, C. (2005). The biology of the goat. http://www.khimaira.com.

Kido, N., Kamegaya,C., Omiya,T. and Wada, Y.(2011).Hematology and serum

biochemistry in debilitated free ranging raccoon dogs (Nyctereutes procyonoides)

infested with sarcoptic mange. Parasitology International, 60: 425-428.

Kral,F. and Schwartzman,R.M .(1964).Veterinary and Comparative Dermatology. J.B.

Lippinncott Company, Philadelphia, Pennsylvania, pp 343-368.

Kumar,A., Vihan,V.S., Sadhana,N. and Sharma,H.N. (2010). Hematological and

biochemical effects of tick infestation in common Indian goat. Advances in

Bioresearch, 1(1): 163-168.

Lastras, M.E., Pastor, J., Marco, I., Ruiz, M., Vinas, L. and Lavin, S. (2000). Effects of

sarcoptic mange on serum proteins and immunoglobin G levels in chamois

(Rupricapra pyrenaica) and Spanish ibex (Capra pyrenaica).Veterinary

Parasitology, 88(3-4):313-319.

Leon-Vizcaino, L., Ruiz De Ybafiez, M. R. and Cubero, M. J. (2001).Sarcoptic mange in

Spanish ibex from Spain. Journal of Wildlife Diseases, 35(4): 647-659.

Little, S.E., Davidson, W.R., Rakich, P.M., Nixon, T.L., Bounous, D.I and Nettle, V.F.

(1998). Responses of red foxes to first and second infection with Sarcoptes

scabiei. Journal of Wildlife Diseases, 34: 600-611.

Lubran, M.M. (1978). The measurement of total serum protein by the Biuret method.

Annals of Clinical Laboratory Science, 8(2): 106-110.

83

Lughano, K. and Dominic, K. (2006). Diseases of small ruminants: A handbook of

common diseases of sheep and goats in sub-Saharan Africa. International

Managers of the Livestock Production Programme(LLP) funded by DFID.

Manurung,J., Stevenson,P., Beriajaya,P. and Knox,M.R.(1990).Use of invermectin to

control sarcoptic mange in goats in Indonesia.Tropical Animal Health and

Production, 22(3):206-212.

Mattsson, J. G., Ljunggren, E.L.,and Bergstrom,K. (2001).Paramyosin from the parasitic

mite Sarcoptes scabiei: cDNA cloning and heterologous expression. Parasitology,

122:555-562.

McCarthy,J. S., Kemp,T.D.J., Walton,S.F. and Currie,B.J.(2004). Scabies: more than just

an irritation. Postgraduate Medical Journal, 80:382-387.

Mellanby, K. (1944). The development of symptoms, parasitic infection and immunity in

human scabies. Parasitology, 35:197-206.

Mercks Veterinary Manual. (2011).Mange in sheep and goats. Merck Sharp and Dohme

Carp., A subsidiary of Merck and Co. Inc., White house station, NJ. USA.

Micali, G., Lacarrubba, F. and Tedeschi,A. (2004).Videodermatoscopy enhances the

ability to monitor efficacy of scabies treatment and allows optimal timing of drug

application. Journal of the European Academy of Dermatology and Venereology,

18:153-154.

Minjauw, B. and Mcleod, A. (2003). Tick born disease and poverty. The impact of ticks

and tick borne diseases in India and South Africa. Research report. DFID Animal

Health Programme,Centre for Tropical Veterinary Medicine, University of

Edinburgh, U.K. 1-116.

Montesu, M. A. and Cottoni,B. (1991). Bonomo F.G.C. and Cestoni,D: Discoverers of the

parasitic origin of scabies. American Journal of Dermatopathology, 13:425-427.

Morgan, M.S., Arlian, L.G. and Estes,S.A.(1997).Skin test and radioallergosorbent test

characteristics of scabietic patients. American Journal of Tropical Medicine and

Hygiene, 57:190-196.

Morris, D.O. and Dunstan, R. W. (1996). A histomorphological study of sarcoptic

acariasis in the dog: 19 cases. Journal of the American Animal Hospital

Association, 32(2): 119-124.

Morsy, G.H. and Gaafar, S.M. (1989). Responses of immunoglobulin-secreting cells in

the skin of pigs during Sarcoptes scabiei infestation. Veterinary Parasitology, 33:

165-175.

Nakagawa,T.L., Takai,Y., Kubo,M., Sakai,H., Masegi,T. and Yanai, T. (2009). A

pathological study of sepsis associated with sarcoptic mange in raccoon dogs

(Nyctereutes procyonoides) in Japan.Journal of Comparative Pathology, 141: 177

-181.

84

Nektarios,D.G., Rania,F., Nikolaos,P., Papadopoulos,E., Karatzias,H. and Alexander,F.

K.(2011).Moxidectin efficacy in a goat herd with chronic and generalized

sarcoptic mange. Veterinary Medicine International, 45-50.

Neeld, J.B.(Jr). and Pearson, W.N. (1963). Macro and micromethods for the

determination of serum vitamin A using trifluoroacetic acid. Journal of Nutrition,

79:454.

Ninomiya,H. and Ogata, M. (2005). Sarcoptic mange in free-ranging raccoon dogs

(Nyctereutes procyonoides) in Japan, Veterinary Dermatology, 16:177-182.

Nwoha, R.I.O. (2011). A case report on scabies in a goat. Clinical Reviews and Opinion,

3 (5): 51-54.

Oishi, S. (2002). Effects of propylparaben on the male reproductive system. Food

Chemicals and Toxicology, 40: 1807-1813.

Okewole,E.A. (1997).Effect of feed supplementation on the management of caprine

sarcoptic mange using ivermectin for treatment. Proceedings and Abstracts of the

34th

Annual Congress of the Nigerian Veterinary Medical Association, pp 2.

Olubunmi,K. (1995). The prevalence of caprine sarcoptic mange due to sarcoptes scabie

var capri in Ile-Ife Area of Ngeria,its control and management. Bulletin of Animal

Health and Production in Africa, 45:155-119.

Overskaug,K. Behavioral changes in free ranging red foxes (Vulpes vulpes) due to

sarcoptic mange. Acta Veterinaria Scandinavca, 26:457-459.

Parmar, A.J., Singh, V., Chaudhary, S.S., Prajapati, B.H. and Sengar, Y.S. (2005).

Hematobiochemical studies on sarcoptic mange in camel (Camelus dromedarus)

in Banaskantha district (North Gujarat). Journal of Parasitic Diseases. 29 (1): 71-

73.

Pence, D.B. and Ueckermann,E.(2002).Sarcoptic mange in wildlife. Revue Scientifique et

Technique Office International des. Epizootics, 21:385-398.

Pence, D. B., Windberg, L. A., Pence, B. C. and Sprowls ,R. (1983). The epizootiology

and pathology of sarcoptic mange in coyotes (Canis latrans) from south Texas.

The Journal of Parasitology, 69: 1100-1115.

Prashad,J.(1984).Studies on some aspects of scabies in goats and calves. Indian

Veterinary Journal, 61:329-343.

Radostits, O.M., Gay, C.C., Blood, D.C. and Hincheliff, K.W. (2000).Veterinary

Medicine:A textbook of the diseases of cattle, sheep, pig, goats and horses.

9th

Edn: 1411-1412.

85

Rambozzi,L., Menzano, A., Molinar-Min,A.R. and Rossi, L. (2007).Immunoblot analysis

of IgG antibody response to Sarcoptes scabiei in swine.Veterinary Immunology

and Immunopathology, 15: 179-183.

Ramos-e-Silva, M.(1998). Giovan Cosimo Bonomo (1663-1696): Discoverer of the

etiology of scabies. International Journal of Dermatology, 37:625-630.

Rantanen, T., Bjorksten, F., Reunala, T. and Salo, O.P.(1981).Serum IgE antibodies to

scabies mite. Acta Dermatologia and Venereologia, 61: 358-360.

Rapp, C.M., Morgan, M.S. and Arlian, I.G. (2006). Presence of host immunoglobulin in

the gut of Sarcoptes scabiei (Acari:Sarcoptidae). Journal of Medical Entomology,

43:539-542.

Rehbein, S., Visser, M., Winter, R., Trommer, B., Matthes, H.F., Maciel A.E. and

Marley, S.E. (2003). Productivity effects of bovine mange and its control with

ivermectin. Veterinary Parasitology, 114:267-284.

Reunala,T., Ranki,A., Rantanen,T. and Salo, O.P.(1984). Inflammatory cells in skin

lesions of scabies. Clinical and Experimental Dermatology, 9: 70-77.

Rhodes, A. P. (1976). The effect of extensive chorioptic mange of the scrotum on

reproductive function of the ram. Australian Veterinary journal, 512: 250-257

Roberts, L.J., Hulfam, S. E., Walton, S.F. and Currie,B.J. (2005). Crusted scabies: clinical

and immunological findings in seventy-eight patients and a review of the

literature. Journal of Infection, 50:37-381.

Scott, D.W. (1988). Large Animal Dermatology, W.B Saunders, Philadelphia, Pa, USA.

Sheahan, B.J., (1975). Pathology of Sarcoptes scabiei infection in pigs. I. Naturally

occurring and experimentally induced lesions. Journal of Comparative

Pathology, 85: 87-95.

Shoyinka,S.V.O., Chah,K.F., Onyenwe,I.W.O., Eze,D.C. and Onoja,I.R. (2009).Mange in

the West African Dwarf Goats of South Eastern Nigeria: Prevalence and

ivermectin efficacy. Abstracts of the 46th

Annual Congress of the Nigerian

Veterinary Medical Association,20th-24th

October, Awka, Nigeria. pp 124 -125

Skerrat, L.F. (2003).Cellular response in the dermis of common wombats (Vombatus

ursinus) infected with Sarcoptes scabiei var wombati, Journal of Wildlife

Diseases, 35: 633-646.

Skerrat, L.F., Middleton, D. and Beveridge, I. (1999). Distribution of life cycle stages of

Sarcoptes scabiei and effects of severe mange on common wombats in Victoria.

Journal of Wildlife Diseases, 35: 633-646.

Smith, M.C. and Sherman, D.M. (1994). Goat Medicine, Lea and Febiger, Philadelphia,

Pa, USA.

86

Soulsby, E.J.L (1998). Helminths, Arthropods and Protozoa of Domestic Animals,

Bailliere, Tindall and Easel Ltd, London. 465-469.

Strumia,M (1963). A rapid universal blood strain “May-Graunwald-Giemsa” in one

solution. Journal of Laboratory Clinical Medicine, 21: 930.

Svartman, M., Potter, E. V., Finklea, J. F., Poon-King, T. and Earle, D.

E.(1972).Epidemic scabies and acute glomerulonephritis in Trinidad. Lancet, 1:

249-51.

Tarigan,S.(2002). Dermatopathology of caprine scabies and protective immunity in

sensitized goats against Sarcoptes scabiei reinfestation. Jurnal llmu Ternak dan

Veteriner, 7:265-271.

Tally, J. and Sparks, D. (2012). External parasites of goats. Oklahoma Cooperative

Extension Service. EPP-7019. http://osufacts.okstate.edu.

Terry, C. (2011). What are the treatments for mange in goats.www.eHow.com/list

6797517 treament-mange-goats.html.

Thoday, K. L. (1993): Serum Immunoglobulin Concentration in Canine Scabies.

In:Advances in Veterinary Dermatology, Pergamon Press, Oxford, 2:221-227.

Thomson, R.G. (1988). Special Veterinary Pathology, 5

th Ed, B.C. Decker, Inc. Toronto.

Tiez, N.W. (1995). Clinical guide to laboratory Tests, 3rd

ed. Philadelphia,WA Saunders

Co.

Ujjwal, D. and Dey, S. (2010). Evaluation of organ function and oxidant/antioxidant

status in goats with sarcoptic mange. Tropical Animal Health and Production,

48(8):1663-1668.

Urquhart, G.M., Amour, J., Dunkan, J.L., Dunn, A.M. and Jennings, W. (1996).

Veterinary Parasitology, 2nd

Ed. Blackwell Science Limited, Osueymend, Oxford,

London, UK: 180-210.

Van Neste, D.J.J.(1987). Scabies in the pig as a model of human scabies with special

reference to the hyperkeratotic form of the disease process. Models in

Dermatology, 3: 170-179.

Van Neste, D.J.J. and Lachapelle, J.M.(1981). Host-parasite relationships in

hyperkeratotic (Norwegian) scabies: pathological and immunological findings.

British Journal of Dermatology, 105: 667-678.

Van Neste, D.J.J. and Staquet, M.J.(1986). Similar epidermal changes in hyperkeratotic

scabies of humans and pigs. American Journal of Dermatopathology, 8: 267-273.

87

Walton, S., LowChoy,J., Bouses, A., Valle, A., McBroom, J., Taplin,D., Arlian, L.,

Mathews, J., Currie, B. and Kemp,D. (1999).Genetically distinct dog-derived and

human-derived Sarcoptes scabiei in scabies-endemic communities in northern

Australia. American Journal of Tropical Medicine and Hygiene, 61:542-547.

Walton, S.F. and Currie, B.J. (2007). Problems in diagnosing scabies: A global disease in

human and animal population. Clinical Microbiology Review, 20:268-279.

Walton, S.F., Holt, D.C., Currie, B.J. and Kemp, D.J.(2004). Scabies: New future for a

neglected disease. Advances in Parasitology, 57:309 – 376.

Willis, C., Fischer, K., Walton, S.F., Currie, B.J. and Kemp,D.J.(2006). Scabies mite

inactivated serine protease paralogues are present both internally in the mite gut

and externally in feces. American Journal Tropical Medicine and Hygiene

,75:683-687.

Wondwossen, K., Sefinew, A., Wudu, T., Haileleul, N. and Hailu,M. (2010).Study on

prevalence and effect of diazinon on goat mange in Northeastern Ethiopia. Global

Veterinaria, 5 (5):287-290.

Woodley, D. and Saurat,J.H. (1981). The Burrow Ink Test and the scabies mite. Journal

of the American Academy of Dermatology, 4:715-722.

Yeruham, S., Rosen, A., Hadani, B.and Nyska, A. (1996).Sarcoptic mange in wild

ruminants in zoological gardens in Israel. Journal of Wildlife Diseases, 32(1):57-

61.